Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Promoter-specific RNA polymerase II transcription factor that binds to the GC box, one of the upstream promoter elements, in mammalian cells. The binding of Sp1 is necessary for the initiation of transcription in the promoters of a variety of cellular and viral GENES.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Processes that stimulate the GENETIC TRANSCRIPTION of a gene or set of genes.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.
A family of DNA-binding transcription factors that contain a basic HELIX-LOOP-HELIX MOTIF.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
A multiprotein complex composed of the products of c-jun and c-fos proto-oncogenes. These proteins must dimerize in order to bind to the AP-1 recognition site, also known as the TPA-responsive element (TRE). AP-1 controls both basal and inducible transcription of several genes.
Proteins which maintain the transcriptional quiescence of specific GENES or OPERONS. Classical repressor proteins are DNA-binding proteins that are normally bound to the OPERATOR REGION of an operon, or the ENHANCER SEQUENCES of a gene until a signal occurs that causes their release.
Established cell cultures that have the potential to propagate indefinitely.
A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.
Proteins encoded by homeobox genes (GENES, HOMEOBOX) that exhibit structural similarity to certain prokaryotic and eukaryotic DNA-binding proteins. Homeodomain proteins are involved in the control of gene expression during morphogenesis and development (GENE EXPRESSION REGULATION, DEVELOPMENTAL).
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A large superfamily of transcription factors that contain a region rich in BASIC AMINO ACID residues followed by a LEUCINE ZIPPER domain.
A family of DNA binding proteins that regulate expression of a variety of GENES during CELL DIFFERENTIATION and APOPTOSIS. Family members contain a highly conserved carboxy-terminal basic HELIX-TURN-HELIX MOTIF involved in dimerization and sequence-specific DNA binding.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A family of zinc finger transcription factors that share homology with Kruppel protein, Drosophila. They contain a highly conserved seven amino acid spacer sequence in between their ZINC FINGER MOTIFS.
The so-called general transcription factors that bind to RNA POLYMERASE II and that are required to initiate transcription. They include TFIIA; TFIIB; TFIID; TFIIE; TFIIF; TFIIH; TFII-I; and TFIIJ. In vivo they apparently bind in an ordered multi-step process and/or may form a large preinitiation complex called RNA polymerase II holoenzyme.
A technique for identifying specific DNA sequences that are bound, in vivo, to proteins of interest. It involves formaldehyde fixation of CHROMATIN to crosslink the DNA-BINDING PROTEINS to the DNA. After shearing the DNA into small fragments, specific DNA-protein complexes are isolated by immunoprecipitation with protein-specific ANTIBODIES. Then, the DNA isolated from the complex can be identified by PCR amplification and sequencing.
Genes whose expression is easily detectable and therefore used to study promoter activity at many positions in a target genome. In recombinant DNA technology, these genes may be attached to a promoter region of interest.
A ubiquitously expressed zinc finger-containing protein that acts both as a repressor and activator of transcription. It interacts with key regulatory proteins such as TATA-BINDING PROTEIN; TFIIB; and ADENOVIRUS E1A PROTEINS.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-6 family members. STAT3 is constitutively activated in a variety of TUMORS and is a major downstream transducer for the CYTOKINE RECEPTOR GP130.
A GATA transcription factor that is expressed in the MYOCARDIUM of developing heart and has been implicated in the differentiation of CARDIAC MYOCYTES. GATA4 is activated by PHOSPHORYLATION and regulates transcription of cardiac-specific genes.
The major sequence-specific DNA-binding component involved in the activation of transcription of RNA POLYMERASE II. It was originally described as a complex of TATA-BOX BINDING PROTEIN and TATA-BINDING PROTEIN ASSOCIATED FACTORS. It is now know that TATA BOX BINDING PROTEIN-LIKE PROTEINS may take the place of TATA-box binding protein in the complex.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
An activating transcription factor that plays a key role in cellular responses to GENOTOXIC STRESS and OXIDATIVE STRESS.
A family of transcription factors characterized by the presence of highly conserved calcineurin- and DNA-binding domains. NFAT proteins are activated in the CYTOPLASM by the calcium-dependent phosphatase CALCINEURIN. They transduce calcium signals to the nucleus where they can interact with TRANSCRIPTION FACTOR AP-1 or NF-KAPPA B and initiate GENETIC TRANSCRIPTION of GENES involved in CELL DIFFERENTIATION and development. NFAT proteins stimulate T-CELL activation through the induction of IMMEDIATE-EARLY GENES such as INTERLEUKIN-2.
A specificity protein transcription factor that regulates expression of a variety of genes including VASCULAR ENDOTHELIAL GROWTH FACTOR and CYCLIN-DEPENDENT KINASE INHIBITOR P27.
The first nucleotide of a transcribed DNA sequence where RNA polymerase (DNA-DIRECTED RNA POLYMERASE) begins synthesizing the RNA transcript.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Motifs in DNA- and RNA-binding proteins whose amino acids are folded into a single structural unit around a zinc atom. In the classic zinc finger, one zinc atom is bound to two cysteines and two histidines. In between the cysteines and histidines are 12 residues which form a DNA binding fingertip. By variations in the composition of the sequences in the fingertip and the number and spacing of tandem repeats of the motif, zinc fingers can form a large number of different sequence specific binding sites.
A family of transcription factors that control EMBRYONIC DEVELOPMENT within a variety of cell lineages. They are characterized by a highly conserved paired DNA-binding domain that was first identified in DROSOPHILA segmentation genes.
An electrophoretic technique for assaying the binding of one compound to another. Typically one compound is labeled to follow its mobility during electrophoresis. If the labeled compound is bound by the other compound, then the mobility of the labeled compound through the electrophoretic medium will be retarded.
An activating transcription factor that regulates expression of a variety of GENES including C-JUN GENES; CYCLIN A; CYCLIN D1; and ACTIVATING TRANSCRIPTION FACTOR 3.
An RNA POLYMERASE II specific transcription factor. It plays a role in assembly of the pol II transcriptional preinitiation complex and has been implicated as a target of gene-specific transcriptional activators.
Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter.
Nucleic acid sequences involved in regulating the expression of genes.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.
A DNA-dependent RNA polymerase present in bacterial, plant, and animal cells. It functions in the nucleoplasmic structure and transcribes DNA into RNA. It has different requirements for cations and salt than RNA polymerase I and is strongly inhibited by alpha-amanitin. EC 2.7.7.6.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
A family of transcription factors that contain regions rich in basic residues, LEUCINE ZIPPER domains, and HELIX-LOOP-HELIX MOTIFS.
Activating transcription factors of the MADS family which bind a specific sequence element (MEF2 element) in many muscle-specific genes and are involved in skeletal and cardiac myogenesis, neuronal differentiation and survival/apoptosis.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
A GATA transcription factor that is found predominately in LYMPHOID CELL precursors and has been implicated in the CELL DIFFERENTIATION of HELPER T-CELLS. Haploinsufficiency of GATA3 is associated with HYPOPARATHYROIDISM; SENSORINEURAL HEARING LOSS; and renal anomalies syndrome.
A GATA transcription factor that is specifically expressed in hematopoietic lineages and plays an important role in the CELL DIFFERENTIATION of ERYTHROID CELLS and MEGAKARYOCYTES.
An essential GATA transcription factor that is expressed primarily in HEMATOPOIETIC STEM CELLS.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in fungi.
A family of DNA-binding proteins that are primarily expressed in T-LYMPHOCYTES. They interact with BETA CATENIN and serve as transcriptional activators and repressors in a variety of developmental processes.
A family of transcription factors that contain two ZINC FINGER MOTIFS and bind to the DNA sequence (A/T)GATA(A/G).
A basic helix-loop-helix leucine zipper transcription factor that regulates the CELL DIFFERENTIATION and development of a variety of cell types including MELANOCYTES; OSTEOCLASTS; and RETINAL PIGMENT EPITHELIUM. Mutations in MITF protein have been associated with OSTEOPETROSIS and WAARDENBURG SYNDROME.
Enzymes that oxidize certain LUMINESCENT AGENTS to emit light (PHYSICAL LUMINESCENCE). The luciferases from different organisms have evolved differently so have different structures and substrates.
A signal transducer and activator of transcription that mediates cellular responses to INTERFERONS. Stat1 interacts with P53 TUMOR SUPPRESSOR PROTEIN and regulates expression of GENES involved in growth control and APOPTOSIS.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Activating transcription factors were originally identified as DNA-BINDING PROTEINS that interact with early promoters from ADENOVIRUSES. They are a family of basic leucine zipper transcription factors that bind to the consensus site TGACGTCA of the cyclic AMP response element, and are closely related to CYCLIC AMP-RESPONSIVE DNA-BINDING PROTEIN.
A subunit of NF-kappa B that is primarily responsible for its transactivation function. It contains a C-terminal transactivation domain and an N-terminal domain with homology to PROTO-ONCOGENE PROTEINS C-REL.
A family of basic helix-loop-helix transcription factors that control expression of a variety of GENES involved in CELL CYCLE regulation. E2F transcription factors typically form heterodimeric complexes with TRANSCRIPTION FACTOR DP1 or transcription factor DP2, and they have N-terminal DNA binding and dimerization domains. E2F transcription factors can act as mediators of transcriptional repression or transcriptional activation.
A cell line derived from cultured tumor cells.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Recurring supersecondary structures characterized by 20 amino acids folding into two alpha helices connected by a non-helical "loop" segment. They are found in many sequence-specific DNA-BINDING PROTEINS and in CALCIUM-BINDING PROTEINS.
The material of CHROMOSOMES. It is a complex of DNA; HISTONES; and nonhistone proteins (CHROMOSOMAL PROTEINS, NON-HISTONE) found within the nucleus of a cell.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.
Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in plants.
A GATA transcription factor that is expressed predominately in SMOOTH MUSCLE CELLS and regulates vascular smooth muscle CELL DIFFERENTIATION.
An activating transcription factor that regulates the expression of a variety of GENES involved in amino acid metabolism and transport. It also interacts with HTLV-I transactivator protein.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
A transcription factor that takes part in WNT signaling pathway where it may play a role in the differentiation of KERATINOCYTES. The transcriptional activity of this protein is regulated via its interaction with BETA CATENIN.
An activating transcription factor that regulates expression of a variety of genes including C-JUN GENES and TRANSFORMING GROWTH FACTOR BETA2.
A protein that has been shown to function as a calcium-regulated transcription factor as well as a substrate for depolarization-activated CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. This protein functions to integrate both calcium and cAMP signals.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
One of several general transcription factors that are specific for RNA POLYMERASE III. It is a zinc finger (ZINC FINGERS) protein and is required for transcription of 5S ribosomal genes.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A conserved A-T rich sequence which is contained in promoters for RNA polymerase II. The segment is seven base pairs long and the nucleotides most commonly found are TATAAAA.
Transcription factors that were originally identified as site-specific DNA-binding proteins essential for DNA REPLICATION by ADENOVIRUSES. They play important roles in MAMMARY GLAND function and development.
Theoretical representations that simulate the behavior or activity of genetic processes or phenomena. They include the use of mathematical equations, computers, and other electronic equipment.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Cellular DNA-binding proteins encoded by the c-jun genes (GENES, JUN). They are involved in growth-related transcriptional control. There appear to be three distinct functions: dimerization (with c-fos), DNA-binding, and transcriptional activation. Oncogenic transformation can take place by constitutive expression of c-jun.
Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.
A family of transcription factors that share a unique DNA-binding domain. The name derives from viral oncogene-derived protein oncogene protein v-ets of the AVIAN ERYTHROBLASTOSIS VIRUS.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A class of proteins that were originally identified by their ability to bind the DNA sequence CCAAT. The typical CCAAT-enhancer binding protein forms dimers and consists of an activation domain, a DNA-binding basic region, and a leucine-rich dimerization domain (LEUCINE ZIPPERS). CCAAT-BINDING FACTOR is structurally distinct type of CCAAT-enhancer binding protein consisting of a trimer of three different subunits.
A general transcription factor that is involved in basal GENETIC TRANSCRIPTION and NUCLEOTIDE EXCISION REPAIR. It consists of nine subunits including ATP-DEPENDENT DNA HELICASES; CYCLIN H; and XERODERMA PIGMENTOSUM GROUP D PROTEIN.
A SOXE transcription factor that plays a critical role in regulating CHONDROGENESIS; OSTEOGENESIS; and male sex determination. Loss of function of the SOX9 transcription factor due to genetic mutations is a cause of CAMPOMELIC DYSPLASIA.
An RNA POLYMERASE II specific transcription factor. It may play a role in transcriptional activation of gene expression by interacting with the TATA-BOX BINDING PROTEIN component of TRANSCRIPTION FACTOR TFIID.
Enzymes that catalyze DNA template-directed extension of the 3'-end of an RNA strand one nucleotide at a time. They can initiate a chain de novo. In eukaryotes, three forms of the enzyme have been distinguished on the basis of sensitivity to alpha-amanitin, and the type of RNA synthesized. (From Enzyme Nomenclature, 1992).
A theoretical representative nucleotide or amino acid sequence in which each nucleotide or amino acid is the one which occurs most frequently at that site in the different sequences which occur in nature. The phrase also refers to an actual sequence which approximates the theoretical consensus. A known CONSERVED SEQUENCE set is represented by a consensus sequence. Commonly observed supersecondary protein structures (AMINO ACID MOTIFS) are often formed by conserved sequences.
Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.
Any of the processes by which cytoplasmic or intercellular factors influence the differential control of gene action in bacteria.
A signal transducer and activator of transcription that mediates cellular responses to a variety of CYTOKINES. Stat5 activation is associated with transcription of CELL CYCLE regulators such as CYCLIN KINASE INHIBITOR P21 and anti-apoptotic genes such as BCL-2 GENES. Stat5 is constitutively activated in many patients with acute MYELOID LEUKEMIA.
A transcription factor that possesses DNA-binding and E2F-binding domains but lacks a transcriptional activation domain. It is a binding partner for E2F TRANSCRIPTION FACTORS and enhances the DNA binding and transactivation function of the DP-E2F complex.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
Proteins that originate from plants species belonging to the genus ARABIDOPSIS. The most intensely studied species of Arabidopsis, Arabidopsis thaliana, is commonly used in laboratory experiments.
A method for determining the sequence specificity of DNA-binding proteins. DNA footprinting utilizes a DNA damaging agent (either a chemical reagent or a nuclease) which cleaves DNA at every base pair. DNA cleavage is inhibited where the ligand binds to DNA. (from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
A sequence of amino acids in a polypeptide or of nucleotides in DNA or RNA that is similar across multiple species. A known set of conserved sequences is represented by a CONSENSUS SEQUENCE. AMINO ACID MOTIFS are often composed of conserved sequences.
Proteins containing a region of conserved sequence, about 200 amino acids long, which encodes a particular sequence specific DNA binding domain (the T-box domain). These proteins are transcription factors that control developmental pathways. The prototype of this family is the mouse Brachyury (or T) gene product.
Proteins found in any species of fungus.
Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.
DNA-binding motifs formed from two alpha-helixes which intertwine for about eight turns into a coiled coil and then bifurcate to form Y shaped structures. Leucines occurring in heptad repeats end up on the same sides of the helixes and are adjacent to each other in the stem of the Y (the "zipper" region). The DNA-binding residues are located in the bifurcated region of the Y.
A ubiquitously expressed octamer transcription factor that regulates GENETIC TRANSCRIPTION of SMALL NUCLEAR RNA; IMMUNOGLOBULIN GENES; and HISTONE H2B genes.
Nucleotide sequences of a gene that are involved in the regulation of GENETIC TRANSCRIPTION.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
A plant genus of the family BRASSICACEAE that contains ARABIDOPSIS PROTEINS and MADS DOMAIN PROTEINS. The species A. thaliana is used for experiments in classical plant genetics as well as molecular genetic studies in plant physiology, biochemistry, and development.
Proteins prepared by recombinant DNA technology.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
A general transcription factor that plays a major role in the activation of eukaryotic genes transcribed by RNA POLYMERASES. It binds specifically to the TATA BOX promoter element, which lies close to the position of transcription initiation in RNA transcribed by RNA POLYMERASE II. Although considered a principal component of TRANSCRIPTION FACTOR TFIID it also takes part in general transcription factor complexes involved in RNA POLYMERASE I and RNA POLYMERASE III transcription.
A group of transcription factors that were originally described as being specific to ERYTHROID CELLS.
Screening techniques first developed in yeast to identify genes encoding interacting proteins. Variations are used to evaluate interplay between proteins and other molecules. Two-hybrid techniques refer to analysis for protein-protein interactions, one-hybrid for DNA-protein interactions, three-hybrid interactions for RNA-protein interactions or ligand-based interactions. Reverse n-hybrid techniques refer to analysis for mutations or other small molecules that dissociate known interactions.
A genus of small, two-winged flies containing approximately 900 described species. These organisms are the most extensively studied of all genera from the standpoint of genetics and cytology.
Factors that bind to RNA POLYMERASE III and aid in transcription. They include the assembly factors TFIIIA and TFIIIC and the initiation factor TFIIIB. All combine to form a preinitiation complex at the promotor that directs the binding of RNA POLYMERASE III.
A heterotetrameric transcription factor composed of two distinct proteins. Its name refers to the fact it binds to DNA sequences rich in GUANINE and ADENINE. GA-binding protein integrates a variety of SIGNAL TRANSDUCTION PATHWAYS and regulates expression of GENES involved in CELL CYCLE control, PROTEIN BIOSYNTHESIS, and cellular METABOLISM.
The developmental history of specific differentiated cell types as traced back to the original STEM CELLS in the embryo.
Interacting DNA-encoded regulatory subsystems in the GENOME that coordinate input from activator and repressor TRANSCRIPTION FACTORS during development, cell differentiation, or in response to environmental cues. The networks function to ultimately specify expression of particular sets of GENES for specific conditions, times, or locations.
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
An early growth response transcription factor that has been implicated in regulation of CELL PROLIFERATION and APOPTOSIS.
A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.
The sequential correspondence of nucleotides in one nucleic acid molecule with those of another nucleic acid molecule. Sequence homology is an indication of the genetic relatedness of different organisms and gene function.
Deletion of sequences of nucleic acids from the genetic material of an individual.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
A family of low-molecular weight, non-histone proteins found in chromatin.
Proteins found in any species of bacterium.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A transcription factor that takes part in WNT signaling pathway. The activity of the protein is regulated via its interaction with BETA CATENIN. Transcription factor 7-like 2 protein plays an important role in the embryogenesis of the PANCREAS and ISLET CELLS.
An ets proto-oncogene expressed primarily in adult LYMPHOID TISSUE; BRAIN; and VASCULAR ENDOTHELIAL CELLS.
An enzyme capable of hydrolyzing highly polymerized DNA by splitting phosphodiester linkages, preferentially adjacent to a pyrimidine nucleotide. This catalyzes endonucleolytic cleavage of DNA yielding 5'-phosphodi- and oligonucleotide end-products. The enzyme has a preference for double-stranded DNA.
A polynucleotide consisting essentially of chains with a repeating backbone of phosphate and ribose units to which nitrogenous bases are attached. RNA is unique among biological macromolecules in that it can encode genetic information, serve as an abundant structural component of cells, and also possesses catalytic activity. (Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
The biosynthesis of DNA carried out on a template of RNA.
Proteins found in plants (flowers, herbs, shrubs, trees, etc.). The concept does not include proteins found in vegetables for which VEGETABLE PROTEINS is available.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
A basic helix-loop-helix transcription factor that was originally identified in DROSOPHILA as essential for proper gastrulation and MESODERM formation. It plays an important role in EMBRYONIC DEVELOPMENT and CELL DIFFERENTIATION of MUSCLE CELLS, and is found in a wide variety of organisms.
A tissue-specific subunit of NF-E2 transcription factor that interacts with small MAF PROTEINS to regulate gene expression. P45 NF-E2 protein is expressed primarily in MEGAKARYOCYTES; ERYTHROID CELLS; and MAST CELLS.
Transport proteins that carry specific substances in the blood or across cell membranes.
An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
Cellular DNA-binding proteins encoded by the c-fos genes (GENES, FOS). They are involved in growth-related transcriptional control. c-fos combines with c-jun (PROTO-ONCOGENE PROTEINS C-JUN) to form a c-fos/c-jun heterodimer (TRANSCRIPTION FACTOR AP-1) that binds to the TRE (TPA-responsive element) in promoters of certain genes.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
A group of deoxyribonucleotides (up to 12) in which the phosphate residues of each deoxyribonucleotide act as bridges in forming diester linkages between the deoxyribose moieties.
One of several general transcription factors that are specific for RNA POLYMERASE III. TFIIIB recruits and positions pol III over the initiation site and remains stably bound to the DNA through multiple rounds of re-initiation by RNA POLYMERASE III.
Gated transport mechanisms by which proteins or RNA are moved across the NUCLEAR MEMBRANE.
One of the BASIC-LEUCINE ZIPPER TRANSCRIPTION FACTORS that is synthesized as a membrane-bound protein in the ENDOPLASMIC RETICULUM. In response to endoplasmic reticulum stress it translocates to the GOLGI APPARATUS. It is activated by PROTEASES and then moves to the CELL NUCLEUS to regulate GENETIC TRANSCRIPTION of GENES involved in the unfolded protein response.
A family of mammalian POU domain factors that are expressed predominately in NEURONS.
Use of restriction endonucleases to analyze and generate a physical map of genomes, genes, or other segments of DNA.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
A subclass of SOX transcription factors that are expressed in neuronal tissue where they may play a role in the regulation of CELL DIFFERENTIATION. Members of this subclass are generally considered to be transcriptional activators.
Formation of an acetyl derivative. (Stedman, 25th ed)
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
A basic-leucine zipper transcription factor that regulates GLOBIN gene expression and is related to TRANSCRIPTION FACTOR AP-1. NF-E2 consists of a small MAF protein subunit and a tissue-restricted 45 kDa subunit.
Genes which regulate or circumscribe the activity of other genes; specifically, genes which code for PROTEINS or RNAs which have GENE EXPRESSION REGULATION functions.
A heterotrimeric DNA-binding protein that binds to CCAAT motifs in the promoters of eukaryotic genes. It is composed of three subunits: A, B and C.
Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promoter and enhancer regions.
A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)
A species of fruit fly much used in genetics because of the large size of its chromosomes.
A subclass of closely-related SOX transcription factors. Members of this subfamily have been implicated in regulating the differentiation of OLIGODENDROCYTES during neural crest formation and in CHONDROGENESIS.
Ubiquitously expressed basic HELIX-LOOP-HELIX MOTIF transcription factors. They bind CANNTG sequences in the promoters of a variety of GENES involved in carbohydrate and lipid metabolism.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.
Elements of limited time intervals, contributing to particular results or situations.
A family of muscle-specific transcription factors which bind to DNA in control regions and thus regulate myogenesis. All members of this family contain a conserved helix-loop-helix motif which is homologous to the myc family proteins. These factors are only found in skeletal muscle. Members include the myoD protein (MYOD PROTEIN); MYOGENIN; myf-5, and myf-6 (also called MRF4 or herculin).
A DNA-dependent RNA polymerase present in bacterial, plant, and animal cells. It functions in the nucleoplasmic structure where it transcribes DNA into RNA. It has specific requirements for cations and salt and has shown an intermediate sensitivity to alpha-amanitin in comparison to RNA polymerase I and II. EC 2.7.7.6.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The developmental entity of a fertilized egg (ZYGOTE) in animal species other than MAMMALS. For chickens, use CHICK EMBRYO.
The process by which two molecules of the same chemical composition form a condensation product or polymer.
Factors that form a preinitiation complex at promoters that are specifically transcribed by RNA POLYMERASE I.
A basic helix-loop-helix transcription factor that plays a role in determining cell fate during embryogenesis. It forms a heterodimer with TWIST TRANSCRIPTION FACTOR and ACHAETE-SCUTE GENE COMPLEX-related TRANSCRIPTION FACTORS.
Characteristic restricted to a particular organ of the body, such as a cell type, metabolic response or expression of a particular protein or antigen.
Commonly observed structural components of proteins formed by simple combinations of adjacent secondary structures. A commonly observed structure may be composed of a CONSERVED SEQUENCE which can be represented by a CONSENSUS SEQUENCE.
A POU domain factor that regulates expression of GROWTH HORMONE; PROLACTIN; and THYROTROPIN-BETA in the ANTERIOR PITUITARY GLAND.
Process of generating a genetic MUTATION. It may occur spontaneously or be induced by MUTAGENS.
A subclass of closely-related SOX transcription factors. Members of the group have been found expressed in developing neuronal tissue, LYMPHOCYTES, and during EMBRYONIC DEVELOPMENT.

Interleukin-12 induces expression of interferon regulatory factor-1 via signal transducer and activator of transcription-4 in human T helper type 1 cells. (1/357)

IRF-1-deficient mice show a striking defect in the development of T helper 1 (Th1) cells. In the present report, we investigate the expression of IRF-1 during differentiation of human T helper cells. No significant differences of IRF-1 mRNA expression were found in established Th1 and Th2 cells; however, interleukin 12 (IL-12) induced a strong up-regulation of IRF-1 transcripts in Th1 but not in Th2 cells. We demonstrate that IL-12-induced up-regulation of IRF-1 is mediated by signal transducer and activator of transcription-4, which binds to the interferon (IFN)-gamma-activated sequence present in the promoter of the IRF-1 gene. Strong IL-12-dependent activation of a reporter gene construct containing the IRF-1 IFN-gamma-activated sequence element provides further evidence for the key role of signal transducer and activator of transcription-4 in the IL-12-induced up-regulation of IRF-1 transcripts in T cells. IRF-1 expression was strongly induced after stimulation of naive CD4(+) T cells via the T cell receptor, irrespective of the cytokines present at priming, indicating that this transcription factor does not play a major role in initiating a Th1-specific transcriptional cascade in differentiating helper T cells. However, our finding that IRF-1 is a target gene of IL-12 suggests that some of the IL-12-induced effector functions of Th1 cells may be mediated by IRF-1.  (+info)

Homocysteine-induced endoplasmic reticulum stress and growth arrest leads to specific changes in gene expression in human vascular endothelial cells. (2/357)

Alterations in the cellular redox potential by homocysteine promote endothelial cell (EC) dysfunction, an early event in the progression of atherothrombotic disease. In this study, we demonstrate that homocysteine causes endoplasmic reticulum (ER) stress and growth arrest in human umbilical vein endothelial cells (HUVEC). To determine if these effects reflect specific changes in gene expression, cDNA microarrays were screened using radiolabeled cDNA probes generated from mRNA derived from HUVEC, cultured in the absence or presence of homocysteine. Good correlation was observed between expression profiles determined by this method and by Northern blotting. Consistent with its adverse effects on the ER, homocysteine alters the expression of genes sensitive to ER stress (ie, GADD45, GADD153, ATF-4, YY1). Several other genes observed to be differentially expressed by homocysteine are known to mediate cell growth and differentiation (ie, GADD45, GADD153, Id-1, cyclin D1, FRA-2), a finding that supports the observation that homocysteine causes a dose-dependent decrease in DNA synthesis in HUVEC. Additional gene profiles also show that homocysteine decreases cellular antioxidant potential (glutathione peroxidase, NKEF-B PAG, superoxide dismutase, clusterin), which could potentially enhance the cytotoxic effects of agents or conditions known to cause oxidative damage. These results successfully demonstrate the use of cDNA microarrays in identifying homocysteine-respondent genes and indicate that homocysteine-induced ER stress and growth arrest reflect specific changes in gene expression in human vascular EC.  (+info)

Middle T antigen activation of signal transduction pathways does not overcome p53-mediated growth arrest. (3/357)

Polyomavirus middle T antigen does not overcome p53-mediated G(1) arrest in mouse embryo fibroblasts. Middle T antigen still associates with the signaling molecules phosphatidylinositol 3-kinase and SHC and activates the transcriptional activity of c-Myc and AP1 in p53-arrested cells. Examination of cell cycle regulatory proteins indicated that p53 does not interfere with these mitogenic signals but acts later in the G(1) phase of the cell cycle.  (+info)

Heregulin induces expression, DNA binding activity, and transactivating functions of basic leucine zipper activating transcription factor 4. (4/357)

Heregulin beta1 (HRG), a combinatorial ligand for human epidermal growth factor receptor 3 and human epidermal growth factor receptor 4 receptors, is a regulatory secretory polypeptide with distinct biological effects such as growth stimulation, differentiation, invasiveness, and migration in breast cancer cells. The mechanism underlying the diverse functions of HRG is not well established, but it is believed to be dependent on the induced changes in expression of specific cellular gene products, their modification, or both. The binding of basic leucine zipper transcription factors to the cAMP response element is known to activate a variety of gene products with a role or roles in growth regulation. In the studies presented here, we identified basic leucine zipper activating transcription factor (ATF) 4 as one of the HRG-inducible gene product. We demonstrated that HRG stimulation of human cancer cells induces expression of ATF4 mRNA and protein, ATF4 DNA binding activity, and ATF4 transactivating function. Consistent with its role as a transcriptional activator, HRG-stimulated ATF4 protein stimulated the transcription from an artificial promoter with three tandem ATF sites or from a naturally occurring promoter with ATF4 sites such as E-selectin. We also demonstrated a preferential role of the HRG-stimulated mitogen-activated protein kinase pathway, but not the phosphatidylinositol 3'-kinase pathway, in supporting the observed increase in ATF4 DNA binding activity and transcription from E-selectin promoter in HRG-stimulated cells. Because ATF4 binding sites are present in a variety of growth-regulating cellular genes, these findings suggest that the stimulation of ATF4 expression and its transactivating functions may constitute an important mechanism of HRG-mediated regulation of putative genes with diversified functions. The present study is the first demonstration of regulation of expression and transactivation ability of ATF4 by any polypeptide growth factor.  (+info)

Identification and characterization of basal and cyclic AMP response elements in the promoter of the rat GTP cyclohydrolase I gene. (5/357)

5812 base pairs of rat GTP cyclohydrolase I (GTPCH) 5'-flanking region were cloned and sequenced, and the transcription start site was determined for the gene in rat liver. Progressive deletion analysis using transient transfection assays of luciferase reporter constructs defined the core promoter as a highly conserved 142-base pair GC-rich sequence upstream from the cap site. DNase I footprint analysis of this region revealed (5' --> 3') a Sp1/GC box, a noncanonical cAMP-response element (CRE), a CCAAT-box, and an E-box. Transcription from the core promoter in PC12 but not C6 or Rat2 cells was enhanced by incubation with 8-bromo-cyclic AMP. Mutagenesis showed that both the CRE and CCAAT-box independently contribute to basal and cAMP-dependent activity. The combined CRE and CCAAT-box cassette was also found to enhance basal transcription and confer cAMP sensitivity on a heterologous minimal promoter. The addition of the Sp1/GC box sequence to this minimal promoter construct inhibited basal transcription without affecting the cAMP response. EMSA showed that nuclear proteins from PC12 but not C6 or Rat2 cells bind the CRE as a complex containing activating transcription factor (ATF)-4 and CCAAT enhancer-binding protein beta, while both PC12 and C6 cell nuclear extracts were recruited by the CCAAT-box as a complex containing nuclear factor Y. Overexpression of ATF-4 in PC12 cells was found to transactivate the GTPCH promoter response to cAMP. These studies suggest that the elements required for cell type-specific cAMP-dependent enhancement of gene transcription are located along the GTPCH core promoter and include the CRE and adjacent CCAAT-box and the proteins ATF-4, CCAAT enhancer-binding protein beta, and nuclear factor Y.  (+info)

Molecular interactions involved in the transactivation of the human T-cell leukemia virus type 1 promoter mediated by Tax and CREB-2 (ATF-4). (6/357)

The human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription through three 21-bp repeats located in the U3 region of the HTLV-1 long terminal repeat and called Tax-responsive elements (TxREs). Each TxRE contains nucleotide sequences corresponding to imperfect cyclic AMP response elements (CRE). In this study, we demonstrate that the bZIP transcriptional factor CREB-2 is able to bind in vitro to the TxREs and that CREB-2 binding to each of the 21-bp motifs is enhanced by Tax. We also demonstrate that Tax can weakly interact with CREB-2 bound to a cellular palindromic CRE motif such as that found in the somatostatin promoter. Mutagenesis of Tax and CREB-2 demonstrates that both N- and C-terminal domains of Tax and the C-terminal region of CREB-2 are required for direct interaction between the two proteins. In addition, the Tax mutant M47, defective for HTLV-1 activation, is unable to form in vitro a ternary complex with CREB-2 and TxRE. In agreement with recent results suggesting that Tax can recruit the coactivator CREB-binding protein (CBP) on the HTLV-1 promoter, we provide evidence that Tax, CREB-2, and CBP are capable of cooperating to stimulate viral transcription. Taken together, our data highlight the major role played by CREB-2 in Tax-mediated transactivation.  (+info)

Functional analysis of the OCA-B promoter. (7/357)

OCA-B was identified as a B cell-specific coactivator that functions with either Oct-1 or Oct-2 to mediate efficient cell type-specific transcription via the octamer site (ATGCAAAT) both in vivo and in vitro. Mice lacking OCA-B exhibit normal Ag-independent B cell maturation. In contrast, Ag-dependent functions, including production of secondary Ig isotypes and germinal center formation, are greatly affected. To better understand OCA-B expression and, ultimately, the defects observed in the OCA-B knockout mice, we have cloned the OCA-B promoter and examined its function in both transformed and primary B cells. We show here that the OCA-B promoter is developmentally regulated, with activity increasing throughout B cell differentiation. Through physical and functional assays, we have found an activating transcription factor/cAMP response element binding protein binding site (or cAMP response element) that is crucial for OCA-B promoter activity. Furthermore, we demonstrate that IL-4 and anti-CD40 induce both the OCA-B promoter and octamer-dependent promoters, thus implicating OCA-B in B cell signaling events in the nucleus.  (+info)

The cryptocephal gene (ATF4) encodes multiple basic-leucine zipper proteins controlling molting and metamorphosis in Drosophila. (8/357)

The cryptocephal (crc) mutation causes pleiotropic defects in ecdysone-regulated events during Drosophila molting and metamorphosis. Here we report that crc encodes a Drosophila homolog of vertebrate ATF4, a member of the CREB/ATF family of basic-leucine zipper (bZIP) transcription factors. We identified three putative protein isoforms. CRC-A and CRC-B contain the bZIP domain, and CRC-D is a C-terminally truncated form. We have generated seven new crc alleles. Consistent with the molecular diversity of crc, these alleles show that crc is a complex genetic locus with two overlapping lethal complementation groups. Alleles representing both groups were rescued by a cDNA encoding CRC-B. One lethal group (crc(1), crc(R6), and crc(Rev8)) consists of strong hypomorphic or null alleles that are associated with mutations of both CRC-A and CRC-B. These mutants display defects associated with larval molting and pupariation. In addition, they fail to evert the head and fail to elongate the imaginal discs during pupation, and they display variable defects in the subsequent differentiation of the adult abdomen. The other group (crc(R1), crc(R2), crc(E85), crc(E98), and crc(929)) is associated with disruptions of CRC-A and CRC-D; except for a failure to properly elongate the leg discs, these mutants initiate metamorphosis normally. Subsequently, they display a novel metamorphic phenotype, involving collapse of the head and abdomen toward the thorax. The crc gene is expressed throughout development and in many tissues. In third instar larvae, crc expression is high in targets of ecdysone signaling, such as the leg and wing imaginal discs, and in the ring gland, the source of ecdysone. Together, these findings implicate CREB/ATF proteins in essential functions during molting and metamorphosis. In addition, the similarities between the mutant phenotypes of crc and the ecdysone-responsive genes indicate that these genes are likely to be involved in common signaling pathways.  (+info)

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

Word count: 190

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are different types of Breast Neoplasms such as:

1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.

2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.

3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.

4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.

5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.

Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.

Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.

It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

There are several risk factors for developing HCC, including:

* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity

HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:

* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss

If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:

* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope

Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:

* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer

Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.

Some common effects of chromosomal deletions include:

1. Genetic disorders: Chromosomal deletions can lead to a variety of genetic disorders, such as Down syndrome, which is caused by a deletion of a portion of chromosome 21. Other examples include Prader-Willi syndrome (deletion of chromosome 15), and Williams syndrome (deletion of chromosome 7).
2. Birth defects: Chromosomal deletions can increase the risk of birth defects, such as heart defects, cleft palate, and limb abnormalities.
3. Developmental delays: Children with chromosomal deletions may experience developmental delays, learning disabilities, and intellectual disability.
4. Increased cancer risk: Some chromosomal deletions can increase the risk of developing certain types of cancer, such as chronic myelogenous leukemia (CML) and breast cancer.
5. Reproductive problems: Chromosomal deletions can lead to reproductive problems, such as infertility or recurrent miscarriage.

Chromosomal deletions can be diagnosed through a variety of techniques, including karyotyping (examination of the chromosomes), fluorescence in situ hybridization (FISH), and microarray analysis. Treatment options for chromosomal deletions depend on the specific effects of the deletion and may include medication, surgery, or other forms of therapy.

Erythroleukemia typically affects adults in their 50s and 60s, although it can occur at any age. Symptoms may include fever, night sweats, weight loss, and fatigue. The cancer cells can spread to other parts of the body, including the spleen, liver, and lymph nodes.

Erythroleukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore normal blood cell production. In some cases, a bone marrow transplant may be necessary. The prognosis for erythroleukemia is generally poor, with a five-year survival rate of about 20%.

Erythroleukemia is classified as an acute leukemia, meaning it progresses rapidly and can lead to life-threatening complications if left untreated. It is important for patients to receive prompt and appropriate treatment to improve their chances of survival and quality of life.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.

Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.

In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.

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A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.

Genetic Translocation | Definition & Facts | Britannica
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Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.

Translocation, Genetic | health Encyclopedia - UPMC
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A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.

Genetic Translocation | Genetics Home Reference - NIH
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A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.

In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.

Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.

There are several types of liver neoplasms, including:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.

The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.

Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.

Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.

There are several types of melanoma, including:

1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.

The risk factors for developing melanoma include:

1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma

The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:

1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole

If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.

In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.

1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.

Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.

Some common types of eye abnormalities include:

1. Refractive errors: These are errors in the way the eye focuses light, causing blurry vision. Examples include myopia (nearsightedness), hyperopia (farsightedness), astigmatism, and presbyopia (age-related loss of near vision).
2. Amblyopia: This is a condition where the brain favors one eye over the other, causing poor vision in the weaker eye.
3. Cataracts: A cataract is a clouding of the lens in the eye that can cause blurry vision and increase the risk of glaucoma.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss.
5. Macular degeneration: This is a condition where the macula, the part of the retina responsible for central vision, deteriorates, leading to vision loss.
6. Diabetic retinopathy: This is a complication of diabetes that can damage the blood vessels in the retina and lead to vision loss.
7. Retinal detachment: This is a condition where the retina becomes separated from the underlying tissue, leading to vision loss.
8. Corneal abnormalities: These are irregularities in the shape or structure of the cornea, such as keratoconus, that can cause blurry vision.
9. Optic nerve disorders: These are conditions that affect the optic nerve, such as optic neuritis, that can cause vision loss.
10. Traumatic eye injuries: These are injuries to the eye or surrounding tissue that can cause vision loss or other eye abnormalities.

Eye abnormalities can be diagnosed through a comprehensive eye exam, which may include visual acuity tests, refraction tests, and imaging tests such as retinal photography or optical coherence tomography (OCT). Treatment for eye abnormalities depends on the specific condition and may include glasses or contact lenses, medication, surgery, or other therapies.

Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.

There are several different types of neuroblastoma, including:

1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.

Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:

* Abdominal pain
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* Increased heart rate

Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.

Embryonal carcinoma is thought to be caused by genetic mutations that occur during fetal development. These mutations can disrupt the normal growth and development of cells, leading to the formation of abnormal tissue and eventually cancer.

Symptoms of embryonal carcinoma vary depending on the location of the tumor. They may include skin lesions, seizures, developmental delays, and gastrointestinal problems. Diagnosis is typically made through a combination of imaging tests such as ultrasound, CT scans, and MRI scans, as well as biopsy to confirm the presence of cancer cells.

Treatment for embryonal carcinoma usually involves surgery to remove the tumor, as well as chemotherapy and/or radiation therapy to destroy any remaining cancer cells. In some cases, bone marrow or stem cell transplantation may be necessary. Prognosis for this disease is generally poor, as it is often diagnosed at a late stage and can be difficult to treat effectively.

Embryonal carcinoma is different from other types of cancer in that it arises from embryonic tissue rather than adult tissue. It is also characterized by the presence of immature cells, which are not found in more advanced cancers. Overall, embryonal carcinoma is a rare and aggressive form of cancer that requires specialized treatment and management.

1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.

Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).

Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.

There are several types of colonic neoplasms, including:

1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.

Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.

Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.

Examples of experimental liver neoplasms include:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.

The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.

There are several types of osteosarcomas, including:

1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.

The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:

1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.

Symptoms of osteosarcoma may include:

1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone

If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:

1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.

There are several types of lung neoplasms, including:

1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.

Lung diseases can also be classified based on their cause, such as:

1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.

Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.

Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:

1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)

The symptoms of adenocarcinoma depend on the location of the cancer and can include:

1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)

The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.

Treatment options for adenocarcinoma depend on the location of the cancer and can include:

1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.

The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.

Medical Term: Cardiomegaly

Definition: An abnormal enlargement of the heart.

Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.

Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.

Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.

Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.

Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

Ewing's sarcoma is a rare and aggressive type of cancer that affects the bones and soft tissues of the body. It primarily occurs in the pelvis, spine, and limbs. This malignancy usually develops in children and young adults between the ages of 10 and 30.

Ewing's sarcoma is caused by a genetic mutation in the EWS gene, which is responsible for regulating cell growth and division. The mutated gene leads to uncontrollable cell proliferation, resulting in the formation of a tumor.

The symptoms of Ewing's sarcoma vary depending on the location of the tumor but can include pain, swelling, limited mobility, and broken bones. Diagnosis is usually made through a combination of imaging tests such as X-rays, CT scans, and PET scans, along with a biopsy to confirm the presence of cancer cells.

Treatment for Ewing's sarcoma typically involves a combination of surgery, chemotherapy, and radiation therapy. Surgery is used to remove the tumor and any affected tissue, while chemotherapy and radiation therapy are used to kill any remaining cancer cells. The prognosis for Ewing's sarcoma varies depending on the stage and location of the cancer but can be improved with early diagnosis and appropriate treatment.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."


There are several subtypes of carcinoma, including:

1. Adenocarcinoma: This type of carcinoma originates in glandular cells, which produce fluids or mucus. Examples include breast cancer, prostate cancer, and colon cancer.
2. Squamous cell carcinoma: This type of carcinoma originates in squamous cells, which are found on the surface layers of skin and mucous membranes. Examples include head and neck cancers, cervical cancer, and anal cancer.
3. Basal cell carcinoma: This type of carcinoma originates in the deepest layer of skin, called the basal layer. It is the most common type of skin cancer and tends to grow slowly.
4. Neuroendocrine carcinoma: This type of carcinoma originates in cells that produce hormones and neurotransmitters. Examples include lung cancer, pancreatic cancer, and thyroid cancer.
5. Small cell carcinoma: This type of carcinoma is a highly aggressive form of lung cancer that spreads quickly to other parts of the body.

The signs and symptoms of carcinoma depend on the location and stage of the cancer. Some common symptoms include:

* A lump or mass
* Pain
* Skin changes, such as a new mole or a change in the color or texture of the skin
* Changes in bowel or bladder habits
* Abnormal bleeding

The diagnosis of carcinoma typically involves a combination of imaging tests, such as X-rays, CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a small sample of tissue for examination under a microscope. Treatment options for carcinoma depend on the location and stage of the cancer and may include surgery, radiation therapy, chemotherapy, or a combination of these.

In conclusion, carcinoma is a type of cancer that originates in epithelial cells and can occur in various parts of the body. Early detection and treatment are important for improving outcomes.

References:

1. American Cancer Society. (2022). Carcinoma. Retrieved from
2. Mayo Clinic. (2022). Carcinoma. Retrieved from
3. MedlinePlus. (2022). Carcinoma. Retrieved from

There are several types of skin neoplasms, including:

1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.

While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.

Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.

Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.

Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.

There are several different types of pathologic neovascularization, including:

* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.

The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.

In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.

Also known as Burkitt's Lymphoma.

Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:

1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.

The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.

Carcinogenesis is the process by which normal cells are transformed into cancer cells. This complex process involves a series of genetic and molecular changes that can take place over a long period of time. The term "carcinogenesis" is derived from the Greek words "carcinoma," meaning cancer, and "genesis," meaning origin or creation.

Carcinogenesis is a multistep process that involves several stages, including:

1. initiation: This stage involves the activation of oncogenes or the inactivation of tumor suppressor genes, leading to the formation of precancerous cells.
2. promotion: In this stage, the precancerous cells undergo further changes that allow them to grow and divide uncontrollably.
3. progression: This stage is characterized by the spread of cancer cells to other parts of the body (metastasis).

The process of carcinogenesis is influenced by a variety of factors, including genetics, environmental factors, and lifestyle choices. Some of the known risk factors for carcinogenesis include:

1. tobacco use
2. excessive alcohol consumption
3. exposure to certain chemicals and radiation
4. obesity and poor diet
5. lack of physical activity
6. certain viral infections

Understanding the process of carcinogenesis is important for developing effective cancer prevention and treatment strategies. By identifying the early stages of carcinogenesis, researchers may be able to develop interventions that can prevent or reverse the process before cancer develops.

Types of Craniofacial Abnormalities:

1. Cleft lip and palate: A congenital deformity that affects the upper jaw, nose, and mouth.
2. Premature fusion of skull bones: Can result in an abnormally shaped head or face.
3. Distraction osteogenesis: A condition where the bones fail to grow properly, leading to abnormal growth patterns.
4. Facial asymmetry: A condition where one side of the face is smaller or larger than the other.
5. Craniosynostosis: A condition where the skull bones fuse together too early, causing an abnormally shaped head.
6. Micrognathia: A condition where the lower jaw is smaller than normal, which can affect breathing and feeding.
7. Macroglossia: A condition where the tongue is larger than normal, which can cause difficulty swallowing and breathing.
8. Oculofacial dysostosis: A condition that affects the development of the eyes and face.
9. Treacher Collins syndrome: A rare genetic disorder that affects the development of the face, particularly the eyes, ears, and jaw.

Causes of Craniofacial Abnormalities:

1. Genetics: Many craniofacial abnormalities are inherited from one or both parents.
2. Environmental factors: Exposure to certain drugs, alcohol, or infections during pregnancy can increase the risk of craniofacial abnormalities.
3. Premature birth: Babies born prematurely are at a higher risk for craniofacial abnormalities.
4. Trauma: Head injuries or other traumatic events can cause craniofacial abnormalities.
5. Infections: Certain infections, such as meningitis or encephalitis, can cause craniofacial abnormalities.

Treatment of Craniofacial Abnormalities:

1. Surgery: Many craniofacial abnormalities can be treated with surgery to correct the underlying deformity.
2. Orthodontic treatment: Braces or other orthodontic devices can be used to align teeth and improve the appearance of the face.
3. Speech therapy: Certain craniofacial abnormalities, such as micrognathia, can affect speech development. Speech therapy can help improve communication skills.
4. Medication: In some cases, medication may be prescribed to manage symptoms associated with craniofacial abnormalities, such as pain or breathing difficulties.
5. Rehabilitation: Physical therapy and occupational therapy can help individuals with craniofacial abnormalities regain function and mobility after surgery or other treatments.

It is important to note that the treatment of craniofacial abnormalities varies depending on the specific condition and its severity. A healthcare professional, such as a pediatrician, orthodontist, or plastic surgeon, should be consulted for proper diagnosis and treatment.

It is also important to remember that craniofacial abnormalities can have a significant impact on an individual's quality of life, affecting their self-esteem, social relationships, and ability to function in daily activities. Therefore, it is essential to provide appropriate support and resources for individuals with these conditions, including psychological counseling, social support groups, and education about the condition.

There are several types of teratomas, including:

1. Mature teratoma: This type of teratoma is made up of well-differentiated tissues that resemble normal tissues. It can contain structures such as hair follicles, sweat glands, and sebaceous glands.
2. Immature teratoma: This type of teratoma is made up of poorly differentiated cells that do not resemble normal tissues. It can contain structures such as cartilage, bone, and nervous tissue.
3. Teratoid mesodermal tumor: This type of teratoma arises from the mesoderm, which is one of the three primary layers of cells in the embryo. It can contain structures such as muscle, bone, and connective tissue.
4. Teratoid endodermal tumor: This type of teratoma arises from the endoderm, which is another primary layer of cells in the embryo. It can contain structures such as glandular tissue and epithelial tissue.

Teratomas are usually benign, but they can sometimes be malignant. Malignant teratomas can spread to other parts of the body and cause serious complications. The treatment of teratomas depends on their type, size, and location, as well as the patient's overall health. Treatment options can include surgery, chemotherapy, and radiation therapy.

In summary, a teratoma is a type of tumor that contains abnormal cells that grow and multiply in an uncontrolled manner, often forming masses or lumps. There are several types of teratomas, and they can occur in various parts of the body. Treatment options depend on the type, size, location, and patient's overall health.

Teratocarcinomas can arise from any of the three layers of germ cells: the spermatogonia, the oögonia, or the primordial germ cells. These tumors are often characterized by a mixture of normal and abnormal tissue, including skin, gastrointestinal tract, and other organs. They can also contain teratomy, which is the presence of immature tissue resembling embryonic tissue.

The diagnosis of teratocarcinoma is based on a combination of clinical, radiological, and pathological findings. Treatment options for teratocarcinoma depend on the location, size, and aggressiveness of the tumor, as well as the patient's age and overall health. Surgery is usually the first line of treatment, followed by radiation therapy or chemotherapy if necessary.

In summary, teratocarcinoma is a rare and complex type of cancer that arises from germ cells and can be either malignant or benign. It is characterized by a mixture of normal and abnormal tissue and requires careful diagnosis and treatment planning to ensure the best possible outcome for the patient.

Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.

Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:

1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.

Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.

Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.

1. Innate immunity: This is the body's first line of defense against infection, and it involves the recognition and elimination of pathogens by cells and proteins that are present from birth.
2. Acquired immunity: This type of immunity develops over time as a result of exposure to pathogens, and it involves the production of antibodies and other immune cells that can recognize and eliminate specific pathogens.
3. Cell-mediated immunity: This is a type of immunity that involves the activation of immune cells, such as T cells and macrophages, to fight off infection.
4. Genetic resistance: Some individuals may have a genetic predisposition to disease resistance, which can be influenced by their ancestry or genetic makeup.
5. Environmental factors: Exposure to certain environmental factors, such as sunlight, clean water, and good nutrition, can also contribute to disease resistance.

Disease resistance is an important concept in the medical field, as it helps to protect against infectious diseases and can reduce the risk of illness and death. Understanding how disease resistance works can help healthcare professionals develop effective strategies for preventing and treating infections, and it can also inform public health policies and interventions aimed at reducing the burden of infectious diseases on individuals and communities.

Physical Features:

* Delayed growth and short stature
* Broad forehead
* Long, narrow face with a wide mouth and full lips
* Wide-set eyes that are often blue or green
* Low-set ears
* Curly or wavy hair

Developmental Features:

* Intellectual disability or cognitive impairment
* Delayed speech and language development
* Difficulty with fine motor skills and hand-eye coordination
* Poor musical ability

Personality Profile:

* Friendly and outgoing personality
* High level of empathy and compassion for others
* Excellent social skills
* Love of music and dance
* Curiosity and playfulness

Causes and Inheritance:

Williams syndrome is caused by a deletion of genetic material from chromosome 7, specifically the q11.23 region. This deletion occurs spontaneously, without a known family history or environmental trigger. The disorder is not inherited in a Mendelian pattern, meaning that it does not follow traditional patterns of inheritance.

Diagnosis:

Williams syndrome can be diagnosed through a combination of physical and developmental assessments, as well as genetic testing. Physical features such as broad foreheads and wide mouths are often present at birth, while developmental delays and cognitive impairments may not become apparent until later in childhood. Genetic testing can confirm the diagnosis by identifying the deletion of genetic material on chromosome 7.

Treatment and Management:

There is no cure for Williams syndrome, but early intervention and specialized management can help individuals with the disorder reach their full potential. Treatment may include:

* Physical therapy to improve fine motor skills and coordination
* Speech and language therapy to improve communication skills
* Occupational therapy to develop daily living skills
* Special education programs tailored to individual needs
* Medications to manage cardiovascular problems, hypertension, and sleep disorders

Prognosis:

The prognosis for individuals with Williams syndrome varies depending on the severity of the symptoms. Some individuals may experience significant developmental delays and cognitive impairments, while others may have fewer or no symptoms. With early intervention and specialized management, many individuals with Williams syndrome can lead fulfilling lives and achieve their full potential.

Inheritance Pattern:

Williams syndrome is not inherited in a Mendelian pattern, meaning that it does not follow traditional patterns of inheritance. The disorder is caused by a spontaneous deletion of genetic material on chromosome 7, and there is no known family history or environmental trigger. Each child of an individual with Williams syndrome has a 50% chance of inheriting the deletion and developing the disorder.

Prenatal Testing:

Prenatal testing for Williams syndrome is available but not routine. The test is typically offered to pregnant women who have a family history of the disorder or who have had a previous child with Williams syndrome. Prenatal testing involves analyzing cells from the developing fetus, usually through chorionic villus sampling (CVS) or amniocentesis.

Genetic Counseling:

Genetic counseling is essential for individuals and families affected by Williams syndrome. A genetic counselor can provide information on the inheritance pattern of the disorder, discuss prenatal testing options, and offer guidance on managing the condition. Genetic counseling can also help families understand the risks and benefits of genetic testing and make informed decisions about their reproductive options.

In conclusion, Williams syndrome is a rare genetic disorder that affects approximately 1 in 10,000 individuals worldwide. It is caused by a spontaneous deletion of genetic material on chromosome 7 and is characterized by developmental delays, cognitive impairments, and cardiovascular problems. Early intervention and specialized management can significantly improve the prognosis for individuals with Williams syndrome. Prenatal testing and genetic counseling are available for families who have a risk of inheriting the disorder. With proper care and support, individuals with Williams syndrome can lead fulfilling lives and achieve their full potential.

The symptoms of microphthalmos may include:

* Small eyes with reduced visual acuity
* Difficulty with depth perception and peripheral vision
* Squinting or crossing of the eyes (strabismus)
* Poor eye movement
* Increased sensitivity to light (photophobia)
* Reduced pupillary reflexes

The causes of microphthalmos can include:

* Genetic mutations or chromosomal abnormalities
* Infections such as rubella, syphilis, or toxoplasmosis during pregnancy
* Maternal exposure to certain medications or chemicals during pregnancy
* Trauma or injury to the eye during fetal development
* Tumors or cysts in the eye or surrounding tissues

Diagnosis of microphthalmos typically involves a comprehensive eye exam, including measurements of the eye's size and visual acuity. Imaging tests such as ultrasound or MRI may also be used to evaluate the structure of the eye and surrounding tissues.

Treatment for microphthalmos depends on the underlying cause and severity of the condition. In some cases, corrective glasses or contact lenses may be sufficient to improve vision. Surgery may be necessary in more severe cases to realign the eyes or remove tumors or cysts. In cases where the microphthalmos is due to a genetic mutation, there may be no effective treatment other than managing the symptoms.

AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.

There are several subtypes of AML, including:

1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.

The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:

* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures

AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:

1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.

Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:

1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.

It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.

There are four types of Waardenburg Syndrome:

Type 1: This is the mildest form of the disorder and is characterized by subtle changes in skin and hair pigmentation and slight hearing loss. Individuals with this type typically have blue or grey eyes and a small amount of white hair.

Type 2: This type is more severe than Type 1 and is characterized by more pronounced pigmentation abnormalities, such as white patches on the skin and hair, as well as significant hearing loss. Individuals with this type often have intense blue or grey eyes and may experience developmental delays.

Type 3: This type is also severe and is characterized by a range of physical symptoms including hearing loss, pigmentation abnormalities, and skeletal deformities such as short stature or joint contractures. Individuals with this type often have unique facial features, such as a broad forehead, narrow eyes, and a long nose.

Type 4: This is the most severe form of Waardenburg syndrome and is characterized by profound hearing loss, significant pigmentation abnormalities, and multiple congenital anomalies such as heart defects or digestive system problems. Individuals with this type often have a short life expectancy and may require extensive medical care throughout their lives.

Inheritance Pattern: Waardenburg syndrome is inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. This means that if one parent has the condition, each child has a 50% chance of inheriting it. However, some forms of the condition may be more severe than others and may require specialized medical care.

Treatment and Management: There is no cure for Waardenburg syndrome, but various treatments can help manage its symptoms. Hearing aids or cochlear implants can help improve hearing, while surgery or physical therapy can help correct skeletal deformities. Regular monitoring by a medical professional is also important to ensure that any related health issues are addressed promptly.

In conclusion, Waardenburg syndrome is a rare genetic disorder that affects the development of pigmentation and hearing in individuals. It can range from mild to severe forms, each with distinct physical characteristics and medical needs. With proper management and care, individuals with Waardenburg syndrome can lead fulfilling lives despite the challenges posed by this condition.



Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.

Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.

Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.

The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.

Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.




There are many potential causes of dehydration, including:

* Not drinking enough fluids
* Diarrhea or vomiting
* Sweating excessively
* Diabetes (when the body cannot properly regulate blood sugar levels)
* Certain medications
* Poor nutrition
* Infections
* Poor sleep

To diagnose dehydration, a healthcare provider will typically perform a physical examination and ask questions about the patient's symptoms and medical history. They may also order blood tests or other diagnostic tests to rule out other conditions that may be causing the symptoms.

Treatment for dehydration usually involves drinking plenty of fluids, such as water or electrolyte-rich drinks like sports drinks. In severe cases, intravenous fluids may be necessary. If the underlying cause of the dehydration is a medical condition, such as diabetes or an infection, treatment will focus on managing that condition.

Preventing dehydration is important for maintaining good health. This can be done by:

* Drinking enough fluids throughout the day
* Avoiding caffeine and alcohol, which can act as diuretics and increase urine production
* Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains
* Avoiding excessive sweating by dressing appropriately for the weather and taking breaks in cool, shaded areas when necessary
* Managing medical conditions like diabetes and kidney disease properly.

In severe cases of dehydration, complications can include seizures, organ failure, and even death. It is important to seek medical attention if symptoms persist or worsen over time.

There are several subtypes of lymphoma, B-cell, including:

1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.

The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.

Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.

Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.

Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.

Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.

There are several types of muscular atrophy, including:

1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.

Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.

There are several types of hypertrophy, including:

1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).

Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.

In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.

The symptoms of choriocarcinoma can vary depending on the location and size of the tumor, but they may include:

* Abnormal vaginal bleeding
* Pelvic pain
* Abdominal pain
* Weakness and fatigue
* Shortness of breath
* Nausea and vomiting

If choriocarcinoma is suspected, a variety of tests may be performed to confirm the diagnosis. These may include:

* Ultrasound: This imaging test uses high-frequency sound waves to create pictures of the uterus and ovaries. It can help doctors identify any abnormal growths or tumors in the area.
* Hysteroscopy: This procedure involves inserting a thin, lighted tube through the cervix to visualize the inside of the uterus. Doctors may use hysteroscopy to collect samples of tissue for testing.
* Laparoscopy: This procedure involves making small incisions in the abdomen and using a thin, lighted tube to visualize the inside of the pelvis. Doctors may use laparoscopy to collect samples of tissue for testing or to remove any tumors that are found.
* Biopsy: In this test, doctors take a small sample of tissue from the uterus and examine it under a microscope for cancer cells.

If choriocarcinoma is confirmed, treatment may involve a combination of surgery, chemotherapy, and radiation therapy. The specific treatment plan will depend on the stage and location of the cancer, as well as the patient's overall health.

Prognosis for choriocarcinoma varies depending on the stage of the cancer when it is diagnosed. In general, the prognosis is good if the cancer is caught early and treated promptly. However, if the cancer has spread to other parts of the body (metastasized), the prognosis may be poorer.

It's important for women who have had a molar pregnancy or choriocarcinoma to follow up with their healthcare provider regularly to ensure that any remaining tissue is removed and to monitor for any signs of recurrence.

PALL is a rare form of leukemia, accounting for only about 5-10% of all cases of acute leukemia. It is most commonly seen in adults between the ages of 40 and 60, although it can occur at any age.

The symptoms of PALL are similar to those of other types of leukemia and may include fatigue, fever, night sweats, weight loss, and an enlarged spleen. The diagnosis of PALL is typically made through a combination of physical examination, medical history, and laboratory tests, including a bone marrow biopsy.

Treatment for PALL usually involves chemotherapy, which can be effective in achieving a complete remission in many cases. In some instances, bone marrow transplantation may also be considered as a form of treatment. The prognosis for PALL is generally poor, with a five-year survival rate of about 20-30%. However, with prompt and appropriate treatment, many people with PALL can achieve long-term remission and a good quality of life.

... , also known as ATF2, is a protein that, in humans, is encoded by the ATF2 gene. This gene ... "Entrez Gene: ATF2 activating transcription factor 2". Ozawa K, Sudo T, Soeda E, Yoshida MC, Ishii S (1991). "Assignment of the ... Activating transcription factor 2 has been shown to interact with C-jun, Casein kinase 2, alpha 1, CREB binding protein, ... "Phosphorylation of two eukaryotic transcription factors, Jun dimerization protein 2 and activation transcription factor 2, in ...
"Activating Transcription Factor 7 Interacting Protein". Retrieved 23 April 2011. "AceView: Homo sapiens complex locus QRICH1, ... Interacting Proteins: ATXN1, Spinocerebellar ataxia type 1 protein, and ATF7IP, activating transcription factor 7-interacting ... ATF7IP is a recruiter protein that couples transcriptional factors to the general transcription apparatus, thereby modulating ... transcription regulation and chromatin formation. QRICH1 is expressed at a high level, 3.3 times the average gene. It is ...
"Entrez Gene: ATF1 activating transcription factor 1". Zucman J, Delattre O, Desmaze C, Epstein AL, Stenman G, Speleman F, ... 1993). "Activating transcription factor-1 can mediate Ca(2+)- and cAMP-inducible transcriptional activation". J. Biol. Chem. ... Sun P, Lou L, Maurer RA (1996). "Regulation of activating transcription factor-1 and the cAMP response element-binding protein ... This gene encodes an activating transcription factor, which belongs to the ATF subfamily and bZIP (basic-region leucine zipper ...
Transcription factor AP4 is a member of the basic helix-loop-helix (bHLH) transcription factors, which bind to the E-box ... activating enhancer binding protein 4), also known as TFAP4, is a protein which in humans is encoded by the TFAP4 gene. ... "Entrez Gene: TFAP4 transcription factor AP-4 (activating enhancer binding protein 4)". Hu YF, Lüscher B, Admon A, et al. (1991 ... "Transcription factor AP-4 contains multiple dimerization domains that regulate dimer specificity". Genes Dev. 4 (10): 1741-52. ...
Activating transcription factor 4 (tax-responsive enhancer element B67), also known as ATF4, is a protein that in humans is ... "Entrez Gene: ATF4 activating transcription factor 4 (tax-responsive enhancer element B67)". Franceschi RT, Ge C, Xiao G, Roca H ... He CH, Gong P, Hu B, Stewart D, Choi ME, Choi AM, Alam J (June 2001). "Identification of activating transcription factor 4 ( ... Activating transcription factor GRCh38: Ensembl release 89: ENSG00000128272 - Ensembl, May 2017 GRCm38: Ensembl release 89: ...
"Entrez Gene: transcription factor AP-2 beta (activating enhancer binding protein 2 beta)". Tsukada S, Tanaka Y, Maegawa H, et ... 2006). "Transcription factor activating enhancer-binding protein-2beta. A negative regulator of adiponectin gene expression". J ... Transcription factor AP-2 beta also known as AP2-beta is a protein that in humans is encoded by the TFAP2B gene. AP-2 beta is a ... 2009). "The transcription factor TFAP2B is associated with insulin resistance and adiposity in healthy adolescents". Obesity ( ...
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Activating transcription factor 3 is a member of the mammalian activation transcription factor/cAMP responsive element-binding ... ATF3 activating transcription factor 3". Chen BP, Wolfgang CD, Hai T (March 1996). "Analysis of ATF3, a transcription factor ... Activating transcription factor ATF3 has been shown to interact with: C-jun, DDIT3 JunD, P53, and SMAD3. GRCh38: Ensembl ... Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ (January 1994). "Activating transcription factor-3 stimulates 3',5'-cyclic ...
"Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143-52. doi: ... "Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143-52. doi: ... Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ (January 1994). "Activating transcription factor-3 stimulates 3',5'-cyclic ... Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ (1994). "Activating transcription factor-3 stimulates 3',5'-cyclic adenosine ...
Activating transcription factor 4 upregulates this gene under metabolic stress conditions in hepatocyte cell lines. A loss of ... Salgado MC, Metón I, Anemaet IG, Baanante IV (2014). "Activating transcription factor 4 mediates up-regulation of alanine ... 1839 (4): 288-96. doi:10.1016/j.bbagrm.2014.01.005. PMID 24418603. Celis K, Shuldiner S, Haverfield EV, Cappell J, Yang R, Gong ...
Zinc finger protein 521 (ZFP521) and activating transcription factor 4 (ATF4) are cofactors of Runx2. Furthermore, in ... Runt-related transcription factor 2 (RUNX2) also known as core-binding factor subunit alpha-1 (CBF-alpha-1) is a protein that ... This protein is a member of the RUNX family of transcription factors and has a Runt DNA-binding domain. It is essential for ... RUNX2 is a key transcription factor associated with osteoblast differentiation. It has also been suggested that Runx2 plays a ...
Phosphorylated STAT6 dimerises and acts as a transcription factor activating many genes, such as eotaxin.[citation needed] ... only activates effectively STAT6. Activated STAT6 molecules form dimers which translocate to the nucleus to bind responsive ... Some recent works is evidencing how a wide range of signals can be actually activated by this receptor (e.g. WNT/β-Catenin, ... Xie M, Wu XJ, Zhang JJ, He CS (October 2015). "IL-13 receptor α2 is a negative prognostic factor in human lung cancer and ...
VegT acts as a transcription factor to activate genes specifying endodermal fate while Vg1 acts as a paracrine factor. β- ... These transcription factors regulate other transcription factors, cell surface molecules with roles in cell adhesion, and other ... β-catenin activates the transcription factor stat3. Stat3 coordinates cell movements during gastrulation and contributes to ... Low levels of dorsal can activate the transcription of rhomboid. Dorsal represses the transcription of zerknüllt, tolloid, and ...
"Muscarinic acetylcholine receptors activate expression of the EGR gene family of transcription factors". The Journal of ... Mitchell R, Robertson DN, Holland PJ, Collins D, Lutz EM, Johnson MS (September 2003). "ADP-ribosylation factor-dependent ... 53 (4): 759-765. doi:10.1124/mol.53.4.759. PMID 9547368. von der Kammer H, Mayhaus M, Albrecht C, Enderich J, Wegner M, Nitsch ... 15 (4): 114-119. doi:10.1016/0165-6147(94)90047-7. PMID 8016895. Brann MR, Ellis J, Jørgensen H, Hill-Eubanks D, Jones SV (1994 ...
Iizuka K, Horikawa Y (August 2008). "ChREBP: a glucose-activated transcription factor involved in the development of metabolic ... mainly by promoting the ChREBP transcription factor in the well-fed state. However, more recent study showed that D-glucose-6- ... "Xylulose 5-phosphate mediates glucose-induced lipogenesis by xylulose 5-phosphate-activated protein phosphatase in rat liver". ... J. 55 (4): 617-24. doi:10.1507/endocrj.k07e-110. PMID 18490833. Dentin, Renaud; Tomas-Cobos, Lidia; Foufelle, Fabienne; Leopold ...
... can function either as an activating or an inhibitory transcription factor depending on its transcription cofactors. IRF4 ... IRF4 is a transcription factor belonging to the Interferon Regulatory Factor (IRF) family of transcription factors. In contrast ... April 1996). "A novel interferon regulatory factor family transcription factor, ICSAT/Pip/LSIRF, that negatively regulates the ... IRF4 is a transcription factor that has been implicated in acute leukemia. This gene is strongly associated with pigmentation: ...
Therefore, transcription factors are crucial for adipogenesis. Transcription factors, peroxis proliferator-activated receptor γ ... a lipid-activated transcription factor". Cell. 79 (7): 1147-56. doi:10.1016/0092-8674(94)90006-x. PMID 8001151. S2CID 54387527 ... other transcription factors function in the progression of differentiation. Adipocyte determination and differentiation factor ... C/EBPs, transcription factors, are members of the basic-leucine zipper class. cAMP, an inducer of adipogenesis, can promote ...
... a novel regulator for induction of activating transcription factor-2 and heme oxygenase-1". The Journal of Biological Chemistry ... by control of the upstream activator of insulin growth factor-1 (IGF-1) and mitogen-activated protein kinase (MAPK) signaling ... 269 (27): 17960-4. doi:10.1016/S0021-9258(17)32403-1. PMID 8027054. McDonagh AF, Palma LA, Schmid R (Jan 1981). "Reduction of ...
In a study by Razaghi et al, amino acid starvation activated the transcription factor Gcn4p, resulting in transcriptional ... Gcn4 is a highly conserved protein and its mammalian homolog is known as activating transcription factor-4 (ATF4). ... Gcn4 is a transcription factor and a "master regulator" for gene expression which regulates close to one tenth of the yeast ... DNA-binding protein Transcription factor Razaghi, Ali; Huerlimann, Roger; Owens, Leigh; Heimann, Kirsten (1 December 2015). " ...
Hsu SH, Hsieh-Li HM, Huang HY, Huang PH, Li H (May 2005). "bHLH-zip transcription factor Spz1 mediates mitogen-activated ...
"DC-STAMP interacts with ER-resident transcription factor LUMAN which becomes activated during DC maturation". Molecular ... 31 (4): 409-16. doi:10.1007/s00774-013-0434-0. PMID 23525827. S2CID 22750579. Hartgers FC, Looman MW, van der Woning B, Merkx ...
"The forkhead transcription factor AFX activates apoptosis by induction of the BCL-6 transcriptional repressor". The Journal of ... The protein encoded by this gene was identified as an interacting corepressor of BCL6, a POZ/zinc finger transcription ... 7 (4): 273-81. doi:10.1093/dnares/7.4.271. PMID 10997877. Tang TT, Dowbenko D, Jackson A, Toney L, Lewin DA, Dent AL, Lasky LA ... 36 (4): 411-6. doi:10.1038/ng1321. PMID 15004558. Beausoleil SA, Jedrychowski M, Schwartz D, Elias JE, Villén J, Li J, Cohn MA ...
... and activating transcription factor 3". Cancer Prevention Research. 4 (1): 116-27. doi:10.1158/1940-6207.CAPR-10-0218. PMC ... Black AR, Black JD, Azizkhan-Clifford J (August 2001). "Sp1 and krüppel-like factor family of transcription factors in cell ... gut-enriched Krüppel-like factor or GKLF) is a member of the KLF family of zinc finger transcription factors, which belongs to ... "Developmental and cell type-specific expression of the zinc finger transcription factor Krüppel-like factor 4 (Klf4) in ...
Ji L, Arcinas M, Boxer LM (1995). "The transcription factor, Nm23H2, binds to and activates the translocated c-myc allele in ... Postel EH, Berberich SJ, Flint SJ, Ferrone CA (1993). "Human c-myc transcription factor PuF identified as nm23-H2 nucleoside ... Co-transcription of this gene and the neighboring upstream gene (NME1) generates naturally occurring transcripts (NME1-NME2) ... 17 (2): 522-4. doi:10.1006/geno.1993.1362. PMID 8406509. Engel M, Véron M, Theisinger B, Lacombe ML, Seib T, Dooley S, Welter C ...
"Oncogenic homeodomain transcription factor E2A-Pbx1 activates a novel WNT gene in pre-B acute lymphoblastoid leukemia". ... An example of this includes the translocation of C-MYC, a gene that encodes a transcription factor that leads to increased cell ... Genetic risk factors may include Down syndrome, Li-Fraumeni syndrome, or neurofibromatosis type 1. Environmental risk factors ... Environmental risk factors are also needed to help create enough genetic mutations to cause disease. Evidence for the role of ...
"The DEXD/H-box RNA helicase RHII/Gu is a co-factor for c-Jun-activated transcription". EMBO J. 21 (3): 451-60. doi:10.1093/ ... "The DEXD/H-box RNA helicase RHII/Gu is a co-factor for c-Jun-activated transcription". EMBO J. 21 (3): 451-60. doi:10.1093/ ... and general transcription. DDX21 has been shown to interact with C-jun. GRCh38: Ensembl release 89: ENSG00000165732 - Ensembl, ... 281 (4): 1006-11. doi:10.1006/bbrc.2001.4446. PMID 11237763. Andersen JS, Lyon CE, Fox AH, Leung AK, Lam YW, Steen H, Mann M, ...
"Virus Infection Induces the Assembly of Coordinately Activated Transcription Factors on the IFN-β Enhancer In Vivo". Molecular ... and human papillomavirus E7 protein share the capacity to disrupt the interaction between transcription factor E2F and the ... Howley and his co-workers created gene maps of many species of papillomaviruses and analyzed their transcription patterns and ... 1 (4): 507-518. doi:10.1016/S1097-2765(00)80051-9. ISSN 1097-2765. PMID 9660935. Huang, L.; Kinnucan, E.; Wang, G.; Beaudenon, ...
"Virus infection induces the assembly of coordinately activated transcription factors on the IFN-beta enhancer in vivo". ... is a member of the interferon regulatory factor family of transcription factors. IRF7 encodes interferon regulatory factor 7, a ... "Interferon regulatory factor-7 synergizes with other transcription factors through multiple interactions with p300/CBP ... "Characterization of the interferon regulatory factor-7 and its potential role in the transcription activation of interferon A ...
Transcription factor AP-2 alpha (Activating enhancer binding Protein 2 alpha), also known as TFAP2A, is a protein that in ... "Entrez Gene: TFAP2A transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)". Mitchell PJ, Wang C, Tjian ... Transcription factor AP-2 alpha is a 52-kD sequence-specific DNA-binding protein that enhances transcription of specific genes ... "RB and c-Myc activate expression of the E-cadherin gene in epithelial cells through interaction with transcription factor AP-2 ...
Heat-shock transcription factors (HSFs) activate heat-shock response genes under conditions of heat or other stresses. HSF4 ... Tu N, Hu Y, Mivechi NF (2006). "Heat shock transcription factor (Hsf)-4b recruits Brg1 during the G1 phase of the cell cycle ... "Entrez Gene: HSF4 heat shock transcription factor 4". Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace ... Transcription factors, All stub articles, Human chromosome 16 gene stubs). ...
... which has been attributed to the activation of specific transcription factors. It also depends on the activity of a protein or ... October 2005). "The contribution of apoptosis-inducing factor, caspase-activated DNase, and inhibitor of caspase-activated ... Caspase-activated DNase (CAD) or DNA fragmentation factor subunit beta is a protein that in humans is encoded by the DFFB gene ... It is also known as caspase activated nuclease (CPAN), dna fragmentation factor 40 (DFF-40), DFF2 and DFFB. Besides, there are ...
Daxx can interact and suppress several transcription factors, such as p53, p73, and NF-κB. Proteins other than transcription ... When the cell is treated with TGF-β, HIPK2, a nuclear kinase, phosphorylates Daxx and the activated Daxx in turn activates the ... the encoded protein functions as a potent transcription repressor that binds to sumoylated transcription factors. Its ... The omnipresence of Daxx in the cell nucleus suggests that the protein may also function as a transcription factor. Although it ...
Many viruses have an RNA genome, such as HIV, which uses reverse transcription to create a DNA template from its viral RNA ... Binding of the hormone to insulin receptors on cells then activates a cascade of protein kinases that cause the cells to take ... These signals are usually in the form of water-soluble messengers such as hormones and growth factors and are detected by ... Proteins are made from amino acids that have been activated by attachment to a transfer RNA molecule through an ester bond. ...
... β-catenin becomes a coactivator for TCF and LEF to activate Wnt genes by displacing Groucho and HDAC transcription repressors. ... Yi ZY, Feng LJ, Xiang Z, Yao H (2011). "Vascular endothelial growth factor receptor-1 activation mediates epithelial to ... On the other hand, a lack of α-catenin can promote aberrant transcription, which can lead to cancer. As a result, it can be ... Keratinocytes engineered to not express alpha-catenin have disrupted cell adhesion and activated NF-κB. A tumor cell line with ...
Splicing factor, arginine/serine-rich 6 is a protein that in humans is encoded by the SFRS6 gene. The protein encoded by this ... Ramchatesingh J, Zahler AM, Neugebauer KM, Roth MB, Cooper TA (September 1995). "A subset of SR proteins activates splicing of ... Monsalve M, Wu Z, Adelmant G, Puigserver P, Fan M, Spiegelman BM (August 2000). "Direct coupling of transcription and mRNA ... The encoded nuclear protein belongs to the splicing factor SR family and has been shown to bind with and modulate another ...
June 2012). "Nucleophosmin (NPM1/B23) interacts with activating transcription factor 5 (ATF5) protein and promotes proteasome- ... This protein is deactivated by binding ATP, and activated by its dephosphorylation to ADP, which requires a potassium ion to ... Rauch JN, Gestwicki JE (January 2014). "Binding of human nucleotide exchange factors to heat shock protein 70 (Hsp70) generates ... Rauch JN, Gestwicki JE (January 2014). "Binding of human nucleotide exchange factors to heat shock protein 70 (Hsp70) generates ...
IFNs activate signal transducer and activator of transcription (STAT) complexes; STATs are a family of transcription factors ... As a result, an IFN-stimulated gene factor 3 (ISGF3) complex forms-this contains STAT1, STAT2 and a third transcription factor ... Type I IFNs further activate p38 mitogen-activated protein kinase (MAP kinase) to induce gene transcription. Antiviral and ... this receptor activates the transcription factors IRF3 and NF-κB, which are important for initiating synthesis of many ...
... represses the transcription of the transforming growth factor beta type II receptor by a mechanism involving activator protein ... "Identification and characterization of a novel activated RhoB binding protein containing a PDZ domain whose expression is ... Arthur WT, Ellerbroek SM, Der CJ, Burridge K, Wennerberg K (November 2002). "XPLN, a guanine nucleotide exchange factor for ... Gampel A, Parker PJ, Mellor H (September 1999). "Regulation of epidermal growth factor receptor traffic by the small GTPase ...
Phosphorylation of the transcription factor may activate it and that activated transcription factor may then activate the ... An activated enhancer begins transcription of its RNA before activating a promoter to initiate transcription of messenger RNA ... Several cell function specific transcription factors (there are about 1,600 transcription factors in a human cell) generally ... which enable activating transcription factors to recruit RNA polymerase. As promoters are typically immediately adjacent to the ...
The expression profiles of these transcription factors are driven by the transcription factors that peak in the prior phase, ... them from transcription), activating E2F. Activation of E2F results in transcription of various genes like cyclin E, cyclin A, ... One screen of single-gene knockouts identified 48 transcription factors (about 20% of all non-essential transcription factors) ... of cell cycle transcription factors by Cdk1 may alter the localization or activity of the transcription factors in order to ...
This may be due to BadA's inducing the transcription of proangiogenic factors, as it activates of NF-κB as well as hypoxia- ... In essence, they are virulence factors, factors that make the bacteria harmful and infective to the host organism. TAAs are ... All Trimeric Autotransporter Adhesins are crucial virulence factors that cause serious disease in humans. The most-studied and ... YadA bacterial adhesin protein domain Type V secretion system Virulence factor Cell adhesion Outer membrane Gram negative ...
... users with access to smartphones may also activate the on-screen braille input keyboard, to type braille symbols on to ... Some portions of the transcription rules are not fully codified and rely on the judgment of the transcriber. Thus, when the ... There are numerous factors that influence access to braille literacy, including school budget constraints, technology ... Holland, B. F. (1934). "Speed and Pressure Factors in Braille Reading", Teachers Forum, Vol. 7. pp. 13-17 Lowenfield, B.; Abel ...
... phosphorylates INSIG to activate SREBP and lipogenesis in cancer cells. Lu demonstrated that growth factor receptor activation ... "PKM2 phosphorylates histone H3 and promotes gene transcription and tumorigenesis". Cell. 150 (4): 685-696. doi:10.1016/j.cell. ... In addition, he showed that activation of growth factor receptors, expression of K-Ras G12V and B-Raf V600E, and hypoxia induce ... He also showed that the glycolytic enzyme phosphoglycerate kinase 1 (PGK1) phosphorylates and activates pyruvate dehydrogenase ...
... transcription and transcription factor regulation, cell signaling, histone modification, and DNA repair. Most other UBLs have ... Typically, UBLs are expressed as inactive precursors and must be activated by proteolysis of the C-terminus to expose the ... The process of ubiquitination is a tightly regulated three-step sequence: activation, performed by ubiquitin-activating enzymes ... transcription, DNA repair, RNA splicing, and cellular differentiation. Ubiquitin itself was first discovered in the 1970s and ...
PGD2, PGJ2, Δ12-PGJ2, and 15-deoxy-Δ12,14-PGJ2 activate the transcription factor, PPARγ, with 15-deoxy-Δ12,14-PGJ2 being the ... This PG directly binds with and activates PPARγ thereby inducing the transcription of genes containing the PPARγ response ... KEAP1: cytosolic KEAP1 serves to promote the degradation of Nrf2 by proteasomes thereby inhibiting this transcription factor ... to retain NFκB in the cell cytoplasm thereby inhibiting it from entering the nucleus and acting as a transcription factor (see ...
... the HIF transcription factor is responsible for the expression of a protein. The HIF stabilizer activates the activity of EPO ... Co2+ induces this response by binding to the N-terminus (loop helix loop domain) of the Hypoxia inducing transcription factors ... they cannot then bind and activate transcription of genes encoding Erythropoietin (EPO). With Co2+ stabilization, degradation ... Hypoxia-inducible factor stabilizer (HIF stabilizer) is a pharmaceutical used to treat chronic kidney disease. Like most ...
To further test the role of activated androgen receptors on AHN, flutamide, an antiandrogen drug that competes with ... nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to ... down-regulate adipogenic transcription factors". Endocrinology. 147 (1): 141-54. doi:10.1210/en.2004-1649. PMC 4417624. PMID ... Androgens bind to and activate androgen receptors (ARs) to mediate most of their biological effects. Determined by ...
... /Max dimers activate gene transcription, while Mad/Max and Mnt/Max dimers inhibit the activity of Myc. c-MYC is over ... MYC proto-oncogene, bHLH transcription factor is a protein that in humans is encoded by the MYC gene which is a member of the ... The encoded protein forms a heterodimer with the related transcription factor MAX. This complex binds to the E box DNA ... "MYC MYC proto-oncogene, bHLH transcription factor [ Homo sapiens (human) ]". Retrieved 2020-03-02. Dang CV, McGuire M, Buckmire ...
... to activate the transcription factor NF-κB. Mal (also known as TIRAP) is necessary to recruit Myd88 to TLR 2 and TLR 4, and ... these proteins activate two important transcription factors: NF-κB is a dimeric protein responsible for expression of various ... TLR7 and TLR9 activate both NF-κB and IRF3 through MyD88-dependent and TRIF-independent pathway, respectively. The human ... Another adaptor protein, which is activated by TLR3 and TLR4, is called TIR domain-containing adapter-inducing IFN-β (TRIF). ...
However activated GR can complex with these other transcription factors and prevent them from binding their target genes and ... The biological response depends on the cell type.[citation needed] In the absence of activated GR, other transcription factors ... Chang CJ, Chen YL, Lee SC (October 1998). "Coactivator TIF1beta interacts with transcription factor C/EBPbeta and ... June 1998). "Recruitment of octamer transcription factors to DNA by glucocorticoid receptor". Molecular and Cellular Biology. ...
Accordingly, gene expression by degradation of transcription factors, such as p53, c-jun, c-Fos, NF-κB, c-Myc, HIF-1α, MATα2, ... The proteolytic capacity of 20S core particle (CP) can be activated when CP associates with one or two regulatory particles (RP ... Besides RPs, the 20S proteasomes can also be effectively activated by other mild chemical treatments, such as exposure to low ... gene transcription, signal transduction and apoptosis. Subsequently, a compromised proteasome complex assembly and function ...
It can stimulate transcription factor c‑myc (activation of gene expression) and Ras pathway (suppression of apoptosis). In the ... Granulocyte macrophage colony-stimulating factor (GM-CSF), and IL-6. IL-3 is secreted by basophils and activated T cells to ... Sometimes also called colony-stimulating factor, multi-CSF, mast cell growth factor, MULTI-CSF, MCGF; MGC79398, MGC79399: the ... Activated T cells can either induce their own proliferation and differentiation (autocrine signaling), or that of other T cells ...
Moreover, G6PD is one of a number of glycolytic enzymes activated by the transcription factor hypoxia-inducible factor 1 (HIF1 ... The isoform, G6PDH, is regulated by transcription and posttranscription factors. ... Xu SN, Wang TS, Li X, Wang YP (September 2016). "SIRT2 activates G6PD to enhance NADPH production and promote leukaemia cell ... G6PD is hypomethylated at K403 in acute myeloid leukemia, SIRT2 activates G6PD to enhance NADPH production and promote leukemia ...
However, all other transcription factors in the MSL family-maleless, MSL-1, and MSL-3-are able to act when SXL is not expressed ... SXL is activated to repress increased transcription, while in XY animals SXL is inactive and allows male development to proceed ... In the case of two-fold increased transcription of a single male X chromosome, there is no use for a Barr body, and the male ... These factors act to increase male X chromosome transcriptional activity. Histone acetylation and the consequent upregulation ...
... methylation can lead to the recruitment of transcription factors that repress transcription. Both mechanisms cause the same end ... These pathways are activated in the cellular response to reduce senescence. Mutations resulting in deletion or reduction of ... Regulation of p16 is complex and involves the interaction of several transcription factors, as well as several proteins ... p16 through the interaction of various transcription factors that execute methylation patterns that can repress transcription ...
... and the specific expression of transcription factors has been described, which has provided information on the differential ... Waterman-Storer CM, Worthylake RA, Liu BP, Burridge K, Salmon ED (May 1999). "Microtubule growth activates Rac1 to promote ... Signals sent between the follicular cells and the oocyte (such as factors similar to epidermal growth factor) cause the ... After nucleation, the minus-ends are released and then re-anchored in the periphery by factors such as ninein and PLEKHA7. In ...
Methylated histones can either repress or activate transcription as different experimental findings suggest, depending on the ... however they may be a contributing factor. For example, down-regulation of methylation of lysine 9 on histone 3 (H3K9me3) has ... Chen D, Ma H, Hong H, Koh SS, Huang SM, Schurter BT, Aswad DW, Stallcup MR (June 1999). "Regulation of transcription by a ... Depending on the site and symmetry of methylation, methylated arginines are considered activating (histone H4R3me2a, H3R2me2s, ...
Fluorescent signal strength depends on many factors such as probe labeling efficiency, the type of probe, and the type of dye. ... July 2012). "The lncRNA Malat1 is dispensable for mouse development but its transcription plays a cis-regulatory role in the ... "In-solution fluorescence in situ hybridization and fluorescence-activated cell sorting for single cell and population genome ... "Microfluidics-assisted fluorescence in situ hybridization for advantageous human epidermal growth factor receptor 2 assessment ...
"Chromosomal localization of mitochondrial transcription factor A (TCF6), single-stranded DNA-binding protein (SSBP), and ... This precursor is activated by proteolytic cleavage of the mitochondrial targeting sequence, thus producing a mature 28-kDa ... 26 (4): 239-57. doi:10.1038/bjc.1972.33. PMC 2008650. PMID 4561027. Zhao ST, Chen M, Li SJ, Zhang MH, Li BX, Das M, Bean JC, ... 4 (6): e666. doi:10.1038/cddis.2013.181. PMC 3698548. PMID 23764847. Seo TW, Lee JS, Yoo SJ (Sep 2014). "Cellular inhibitor of ...
Other molecules identified include the transcription factor RUNX2 which may prevent cancer cells from undergoing apoptosis, the ... and is activated manually by the patient through a switch implanted in the scrotum. The latter is considered the gold standard ... Recent studies demonstrated the involvement of growth factors, such as epidermal growth factor (EGF) and neurotensin in the 5- ... Other factors include a diet high in processed meat and red meat, while the risk from a high intake of milk products is ...
... is a multifunctional transcription regulatory protein in the basic leucine zipper superfamily. ATF4 can be expressed in most if ... Biology of Activating Transcription Factor 4 (ATF4) and Its Role in Skeletal Muscle Atrophy Scott M Ebert 1 2 , Blake B ... Biology of Activating Transcription Factor 4 (ATF4) and Its Role in Skeletal Muscle Atrophy Scott M Ebert et al. J Nutr. 2022. ... Activating transcription factor 4 drives the progression of diabetic cardiac fibrosis. Li Y, He Q, He CY, Cai C, Chen Z, Duan ...
Activating transcription factor 4 regulates mitochondrial content, morphology, and functio Activating transcription factor 4 ... In muscle, the necessity for activating transcription factor 4 (ATF4) and its role in regulating mitochondrial quality control ... ATF4 mediated myotube formation through the regulated expression of myogenic factors, mainly Myc and myoblast determination ... Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Assunto principal: Fator 4 Ativador ...
Here we demonstrate that the transcription factor NFAT controls the program of T cell exhaustion. When expre … ... The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells Gustavo J Martinez 1 , Renata M Pereira 1 , Tarmo ... The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells Gustavo J Martinez et al. Immunity. 2015. . ... Activation of the transcription factor NFAT5 in the tumor microenvironment enforces CD8+ T cell exhaustion. Tillé L, Cropp D, ...
9. Fibroblast growth factor 21 induction by activating transcription factor 4 is regulated through three amino acid response ... cAMP-response element (CRE)-mediated transcription by activating transcription factor-4 (ATF4) is essential for circadian ... biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors ... activating transcription factor 2 and CAAT/enhancer binding protein alpha in cyclic AMP response element-mediated transcription ...
... and nuclear factor kappa B (NF-kappa B). In this study the effect on these redox-sensitive factors by 4-hydroxy-2-nonenal (HNE ... and nuclear factor kappa B (NF-kappa B). In this study the effect on these redox-sensitive factors by 4-hydroxy-2-nonenal (HNE ... The diverging effect of HNE on the two transcription factors is likely related to the demonstrated differential activation ... The diverging effect of HNE on the two transcription factors is likely related to the demonstrated differential activation ...
MeSH Terms: Activating Transcription Factor 4; Cell Line; Cells, Cultured; Cysteine; Eukaryotic Initiation Factor-2; Female; ... treatment groups from both models contained upregulated pathways enriched for genes regulated by the ATF4 transcription factor ...
Distinct spatial Ca2+ signatures selectively activate different NFAT transcription factor isoforms. Molecular Cell. 58(2):232- ... Distinct spatial Ca2+ signatures selectively activate different NFAT transcription factor isoforms. Molecular Cell. 58(2):232- ... Selective recruitment of different Ca2+-dependent transcription factors by STIM1-Orai1 channel clusters. Nature Communications. ... Selective recruitment of different Ca2+-dependent transcription factors by STIM1-Orai1 channel clusters. Nature Communications ...
... metal-activated transcription factor 1), a transcription factor that is required for metal-induced transcription of Mt1, but ... metal-activated transcription factor 1; MTF-1; metallothionein; nuclear factor erythroid 2-related factor 2; Nrf2 ... Induction of metallothionein l by phenolic antioxidants requires metal-activated transcription factor 1 (MTF-1) and zinc. ... These findings establish that phenolic antioxidants activate Mt1 transcription by a zinc-dependent mechanism, which involves ...
Regulation of cellular immunity by activating transcription factor 4.. Mukherjee D; Bercz LS; Torok MA; Mace TA. Immunol Lett; ... Single-Cell RNA Sequencing of Tumor-Infiltrating NK Cells Reveals that Inhibition of Transcription Factor HIF-1α Unleashes NK ... 4. Tumor-specific MHC-II expression drives a unique pattern of resistance to immunotherapy via LAG-3/FCRL6 engagement.. Johnson ...
activating transcription factor 4. increases expression. ISO. cannabigerol results in increased expression of ATF4 mRNA. CTD. ... mitogen-activated protein kinase kinase kinase 5. decreases expression. ISO. cannabigerol results in decreased expression of ... peroxisome proliferator activated receptor alpha. multiple interactions. ISO. cannabigerol binds to and results in increased ... eukaryotic translation initiation factor 2 alpha kinase 3. decreases expression. ISO. cannabigerol results in decreased ...
... activating transcription factor 3; ATF4, activating transcription factor 4; ATM/ATR, ataxia-telangiectasia mutated/ataxia- ... increased level of phosphorylated eukaryotic translation initiation factor 2α, activating transcription factor (ATF)4, ATF3, C/ ... Another pro-apoptotic factor that plays a significant role in I-R-induced apoptosis is transcription factor p53. Silencing of ... 1-MT, 1-DL-methyltryptophan; IDO, indoleamine 2,3-dioxygenase 1; ATF4, activating transcription factor 4; CHOP; C/EBP ...
FGF19 (fibroblast growth factor 19) as a novel target gene for activating transcription factor 4 in response to endoplasmic ... Fibroblast growth factor 21 induction by activating transcription factor 4 is regulated through three amino acid response ... 8. Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of ... Drosophila melanogaster activating transcription factor 4 regulates glycolysis during endoplasmic reticulum stress.. Lee JE; ...
Transcription Factors [D12.776.930] * Basic-Leucine Zipper Transcription Factors [D12.776.930.127] * Activating Transcription ... Activating Transcription Factors [D12.776.260.108.061] * Activating Transcription Factor 1 [D12.776.260.108.061.500] ... Factors [D12.776.930.127.061] * Activating Transcription Factor 1 [D12.776.930.127.061.500] * Activating Transcription Factor 2 ... Activating Transcription Factor 4 Preferred Term Term UI T224964. LexicalTag NON. ThesaurusID NLM (2006). ...
... predicted to be associated with the genes exclusively upregulated in preadipocytes included activating transcription factor 4 ( ... Type I interferon gene induction by the interferon regulatory factor family of transcription factors. Immunity 25, 349-360 ( ... Interestingly, the transcription factors IRF3 and IRF7 are recognized as key regulators of type I IFN gene expression induced ... 3c). Concordantly, the top upstream regulators were predicted to be the transcription factors sterol regulatory element binding ...
Srivastava RK, Li C, Wang Y, Weng Z, Elmets CA, Harrod KS, Deshane JS, Athar M. Activating transcription factor 4 underlies the ... Oxidized Phospholipid OxPAPC Activates TRPA1 and Contributes to Chronic Inflammatory Pain in Mice. PLoS One. 2016;11(11): ... Epub 2016 Mar 4. PubMed PMID: 26952014; PubMed Central PMCID: PMC4821717.. Lam A, Vetal N, Matalon S, Aggarwal S. Role of heme ... 2016 May;40(4):304-9. doi: 10.1093/jat/bkw008. Epub 2016 Feb 23. PubMed PMID: 26912564; PubMed Central PMCID: PMC4834430. ...
... exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. This in … ... Here we show that activating transcription factor 4 (ATF4) ... Here we show that activating transcription factor 4 (ATF4) ... 4 , Hamada M Mokhlis 4 5 , Bulent Ozpolat 4 , Wanja Kildal 2 , Havard Emil Danielsen 2 6 7 8 , Ladan Fazli 9 , Paul S Rennie 9 ... exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. This includes activation ...
Transcription factors downstream of signaling events in the primitive streak. Signaling events activate transcription factors ... In response to signals from Wnt, TGF-β, and FGF family members, cells activate transcription factors that in turn induce EMT ( ... The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumor cells. Nat. Cell Biol. 2:84-89 ... The snail superfamily of zinc-finger transcription factors. Nat. Rev. Mol. Cell Biol. 3:155-166. View this article via: PubMed ...
... the canonical transcription factor activated downstream of SMO, in MB-PDX and DAOY cells cultured in NS conditions. Nuclear Gli ... The activated SMO induces processing of Gli transcription factors into their active form, which subsequently promotes ... Cells were plated at 1-2 cells per well in non-adherent plate and cultured in serum-free medium with growth factors for at ... Cellular Cholesterol Directly Activates Smoothened in Hedgehog Signaling. Cell. 2016;166(5):1176-1187.e14. pmid:27545348 * View ...
Lower expression of activating transcription factors 3 and 4 correlates with shorter progression-free survival in multiple ... Mycobacterium tuberculosis 38-kDa antigen induces endoplasmic reticulum stress-mediated apoptosis via toll-like receptor 2/4. ... Int J Oncol; 2011 Oct; 39(4):981-8. PubMed ID: 21667023. [TBL] ...
... including growth factors, chemokines, and stress, activate AP-1-dependent transcription. The transcriptional activity of c-Jun ... c-Jun is a member of the Jun family containing c-Jun, JunB, and JunD, and is a component of the transcription factor activator ... and ATF family members and binds to and activates transcription at TRE/AP-1 elements (reviewed in 1). Extracellular signals, ... For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle ...
... transcription) factors to proliferate and activate the differentiation programs. In the second maturation phase, the first ... Applicant organizations are strongly encouraged to start the registration process at least four (4) weeks prior to the ... 4) importance of the knowledge to be gained, and 5) data and safety monitoring for clinical trials.. For research that involves ... 4) procedures for limiting discomfort, distress, pain and injury to that which is unavoidable in the conduct of scientifically ...
Tan IIA elevated the protein expression of transcription factors: activating transcription factor 4 (ATF4), nuclear factor ( ... mTOR and MEK/ERK which in turn down-regulated the expression of three transcription factors: AP-1, HIF-1αand NF-κB. As a result ... c-Myc and E2F transcription factor 1 (E2F1). Moreover, Tan IIA inhibited NF-κB signalling and expression of MMP-2 and MMP-9, ... 8). Tan IIA antagonized insulin-like growth factor 1 receptor (IGFR), and decreased production of ROS. Tan IIA induced p70 S6K ...
... a ligand-activated transcription factor [11]. Investigation of the urine metabolic profiles showed significant increases in the ... activated via aryl hydrocarbon receptor (AHR); and apoptotic protease activating factor (Apaf1) were upregulated by tryptamine ... IAA upregulates the eight genes regulated by the transcription factor aryl hydrocarbon receptor (AHR) [78]. The reduction in ... epidermal growth factor. 71. Increased in AD. GenBank: CAA34902.2. interleukin-2 isoform X1. 131. lymphokine. NCBI: XP_ ...
... will ask whether these cleavage products and metabolites directly activate or antagonize ligand-dependent transcription factors ... 4) We will probe the biological (nutritional) function of carotenoid metabolites in multiple ways: (a) we will use cell lines ... relevant amounts of beta-carotene or lycopene as well as by quantitation of steady state concentrations in plasma after 4 weeks ...
The helminth likewise activates the transcription factor Stat6, which elicits downstream changes that induce viruses to move ... In addition, the combination of the virus plus the gene mutation led to a distinct profile of gene transcription. The authors ... conclude that the "virus-plus- susceptibility gene interaction can, in combination with additional environmental factors and ... neurologic trauma or growth factor deprivation" (8, p. 506). ... IL-4), both of which culminate in reactivation of the murine γ- ...
... eIF2a-activating transcription factor 4 (ATF4) pathway, ultimately reducing ERS-induced apoptosis [24]. However, whether Sirt-1 ... and activating transcription factor 6 (ATF6)) and apoptosis-related protein (caspase-3 and C/EBP-homologous protein (CHOP)) in ... Histone deacetylase (HDAC) can modify chromatin structure and regulate transcription factor activity [15]. And sirtuin-1 (Sirt- ... Under stress, GRP78 can activate ERS through PERK, ATF6, and IRE1 [49]. While excessive ERS instead can activate ERS-associated ...
"Peroxisome proliferator-activated receptor gamma and retinoid X receptor transcription factors are released from activated ... "Breaking the mold: transcription factors in the anucleate platelet and platelet-derived microparticles." Frontiers in ... "Peroxisome Proliferator-Activated Receptor g and the Retinoid X Receptor are released from activated human platelets and are ... Murphy P.; Connery C.; Hicks GL.; Blumberg N. "Homologous blood transfusion as a risk factor for postoperative infection after ...
... which means it tells the body to activate or regulate certain genes. ATF4 seems to change skeletal muscle with age, reducing ... which means it tells the body to activate or regulate certain genes. ATF4 seems to change skeletal muscle with age, reducing ...
... peroxysome proliferation activating receptor agonists (which modulate NF-kappaB, the transcription factor that drives the ... Becker stated that brain-derived neurotrophic factor (BDNF), which is expressed throughout the brain and plays an important ... and upregulation of corticotrophin releasing factor in the cortex and other brain structures. ... Future Council meetings will take place June 12-13 and September 18-19, 2013; February 5-6, June 4-5, and September 10-11, 2014 ...
  • In muscle , the necessity for activating transcription factor 4 (ATF4) and its role in regulating mitochondrial quality control (MQC) have yet to be determined. (bvsalud.org)
  • ATF4 mediated myotube formation through the regulated expression of myogenic factors, mainly Myc and myoblast determination protein 1 (MyoD), and suppressed mitochondrial biogenesis basally through peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1α). (bvsalud.org)
  • 3. ATF4, an ER stress and hypoxia-inducible transcription factor and its potential role in hypoxia tolerance and tumorigenesis. (nih.gov)
  • 5. Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element. (nih.gov)
  • 7. Understanding of the functional role(s) of the Activating Transcription Factor 4(ATF4) in HIV regulation and production. (nih.gov)
  • 17. cAMP-response element (CRE)-mediated transcription by activating transcription factor-4 (ATF4) is essential for circadian expression of the Period2 gene. (nih.gov)
  • 2. Translational induction of ATF4 during integrated stress response requires noncanonical initiation factors eIF2D and DENR. (nih.gov)
  • 10. Eukaryotic Initiation Factor 5B (eIF5B) Cooperates with eIF1A and eIF5 to Facilitate uORF2-Mediated Repression of ATF4 Translation. (nih.gov)
  • Here we show that activating transcription factor 4 (ATF4) exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. (nih.gov)
  • ATF4 activates proapoptotic genes upon glutamine deprivation in MYC-transformed cells. (aacrjournals.org)
  • Glutamine starvation-induced cell death in MYCN -amplified neuroblastoma cells was dependent on activating transcription factor 4 (ATF4), which directly increased expression of the proapoptotic genes PUMA , NOXA , and TRB3 in response to glutamine deprivation. (aacrjournals.org)
  • Intriguingly, 2 drugs that are well tolerated in humans, epigallocatechin gallate (EGCG), a glutamate dehydrogenase inhibitor, and fenretinide (FRT), a chemotherapeutic agent that activates ATF4, had selective activity against MYCN -amplified neuroblastoma cells whether the drugs were used alone or in combination. (aacrjournals.org)
  • Indeed, it down-regulated the glucose-regulated protein 78 (GRP78), the activating transcription factor 4 (ATF4), the RNA activated protein kinase (PKR)-like ER kinas (PERK), the X box binding protein-1 (XBP-1) and the caspase12 protein levels. (biomedcentral.com)
  • 16. Heregulin induces expression, DNA binding activity, and transactivating functions of basic leucine zipper activating transcription factor 4. (nih.gov)
  • Induction depends on the presence of MTF-1 (metal-activated transcription factor 1), a transcription factor that is required for metal-induced transcription of Mt1, but does not require nuclear factor erythroid 2-related factor 2, a tBHQ-activated CNC bZip (cap 'n' collar basic leucine zipper) protein, that is responsible for regulating genes encoding phase II drug-metabolizing enzymes. (cdc.gov)
  • The related molecular pathway entails tryptophan degradation, general control non‑derepressible‑2 kinase (GCN2K) activation, increased level of phosphorylated eukaryotic translation initiation factor 2α, activating transcription factor (ATF)4, ATF3, C/EBP homologous protein, phosphorylated p53, p53, Bax, death receptor‑5 and eventually activated cleaved caspase‑3. (spandidos-publications.com)
  • Activating transcription factor 4 regulates mitochondrial content, morphology, and function in differentiating skeletal muscle myotubes. (bvsalud.org)
  • 4. Drosophila melanogaster activating transcription factor 4 regulates glycolysis during endoplasmic reticulum stress. (nih.gov)
  • An activating transcription factor that regulates the expression of a variety of GENES involved in amino acid metabolism and transport. (nih.gov)
  • 10. Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)-ATF composite site to regulate Gadd153 expression during the stress response. (nih.gov)
  • 13. Activating transcription factor 4 and CCAAT/enhancer-binding protein-beta negatively regulate the mammalian target of rapamycin via Redd1 expression in response to oxidative and endoplasmic reticulum stress. (nih.gov)
  • 14. Role of basic region leucine zipper transcription factors cyclic AMP response element binding protein (CREB), CREB2, activating transcription factor 2 and CAAT/enhancer binding protein alpha in cyclic AMP response element-mediated transcription. (nih.gov)
  • Phenolic antioxidants, such as tBHQ [2,5-di-(t-butyl)-1,4- hydroquinone ], induce Mt1 (metallothionein 1) gene expression and accumulation of MT protein. (cdc.gov)
  • And fluoride exposure also could downregulate Sirt-1 and upregulate ERS-related proteins (PERK, 78-kD glucose-regulated protein (GRP-78), and activating transcription factor 6 (ATF6)) and apoptosis-related protein (caspase-3 and C/EBP-homologous protein (CHOP)) in rat liver tissues. (fluoridealert.org)
  • Of particular recent interest has been the mitochondrial unfolded protein response (UPR mt ), activated to restore protein homeostasis (proteostasis) upon mitochondrial protein misfolding. (biomedcentral.com)
  • Upon proteostasis failure, stress responses are rapidly activated-typically in a time-course of several hours-in an attempt to alleviate proteostasis defects by modulating the folding environment through modification of protein synthesis and the availability of folding helpers-chaperones (Fig. 1 ). (biomedcentral.com)
  • Secreted Hh protein alters gene transcription by binding the cell-surface receptor Patched (Ptc) preventing repression of the 7 membrane spanning receptor Smoothened (Smo) by Ptc. (bioskinrevive.com)
  • SIGNIFICANCE STATEMENT Similar to microglia, astrocytes become strongly "activated" with neural damage and exhibit numerous morphologic/biochemical changes, including an increase in the expression/activity of the protein phosphatase calcineurin. (jneurosci.org)
  • Hypertrophy of astrocyte somata and processes, along with a corresponding increase in the expression of the glial fibrillary acidic protein (GFAP), are the most robust and recognizable biomarkers of activated astrocytes, yet the functional phenotype of these cells appears highly complex. (jneurosci.org)
  • 2. Transcriptional regulation of activating transcription factor 4 under oxidative stress in retinal pigment epithelial ARPE-19/HPV-16 cells. (nih.gov)
  • Moreover, we have described the primary molecular mechanisms involved in exercise-induced tissue regeneration, including the roles of growth factors, signaling pathways, oxidative stress, metabolic factors, and non-coding RNAs. (springeropen.com)
  • Exercise-promoted stem cell activation could be attributed to several factors such as signaling pathways, oxidative stress, metabolic factors, and non-coding RNAs. (springeropen.com)
  • 17. FGF19 (fibroblast growth factor 19) as a novel target gene for activating transcription factor 4 in response to endoplasmic reticulum stress. (nih.gov)
  • Then, the fluorosis cell model was built, which was also alleviated with NaF, Sirt-1 siRNAs, or endoplasmic reticulum stress (ERS) alleviator (4-PBA). (fluoridealert.org)
  • Increasing evidence suggests that the calcineurin (CN)-dependent transcription factor NFAT (Nuclear Factor of Activated T cells) mediates deleterious effects of astrocytes in progressive neurodegenerative conditions. (jneurosci.org)
  • Using adeno-associated virus (AAV) to inhibit the calcineurin-dependent activation of the transcription factor NFAT (Nuclear Factor of Activated T cells) selectively, we have shown that activated astrocytes contribute to neural dysfunction in animal models characterized by progressive/chronic neuropathology. (jneurosci.org)
  • 8. The molecular biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors: activating transcription factor proteins and homeostasis. (nih.gov)
  • And sirtuin-1 (Sirt-1) is a class III HDAC and can regulate biological processes including cellular metabolism, gene transcription, immune response, and glucose homeostasis through multiple deacetylation factors [ 16 ]. (fluoridealert.org)
  • This activates Gli transcription factors and inactivates their inhibitor Suppressor of Fused (SuFu). (bioskinrevive.com)
  • Ferroptosis triggered by these genes can be inhibited by chemical compounds such as the cystine/glutamate antiporter (System X C - ) inhibitor erastin, the glutathione (GSH) synthesis inhibitor buthionine sulfoximine (BSO), the glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4) inhibitor (1S, 3R)-RSL3, and the glutathione S-transferase inhibitor artesunate (ART) [ 3 , 7 - 11 ]. (oncotarget.com)
  • In the first commitment and proliferation phase, progenitor cells committed to the erythroid lineage are induced by extrinsic (growth) and intrinsic (transcription) factors to proliferate and activate the differentiation programs. (nih.gov)
  • 14. Regulation of cellular immunity by activating transcription factor 4. (nih.gov)
  • In this study, we investigated the role of c-Maf in regulation of the transcription of the p35 gene, which encodes the chain that is rate limiting in the synthesis of the heterodimeric IL-12. (cornell.edu)
  • Activating transcription factor 3: a hormone responsive gene in the etiology of hypospadias. (cdc.gov)
  • However, c-Maf does not appear to be a physiologic regulator of IL-12p40 gene transcription because p40 production is not dysregulated in c-Maf-deficient macrophages. (cornell.edu)
  • The master adipogenic transcription factor PPARgamma cooperates with C/EBPalpha to activate the expression of genes critical for adipogenesis. (nih.gov)
  • 9. Fibroblast growth factor 21 induction by activating transcription factor 4 is regulated through three amino acid response elements in its promoter region. (nih.gov)
  • As articulated by Aranda and Epstein (2015), "Latency is an adaptive phenotype that allows the virus to escape immune host responses and to reactivate and disseminate to other hosts upon recognizing danger signals such as stress, neurologic trauma or growth factor deprivation" (8, p. 506). (oneradionetwork.com)
  • 2019. Selective recruitment of different Ca 2+ -dependent transcription factors by STIM1-Orai1 channel clusters. (nih.gov)
  • The activated SMO induces processing of Gli transcription factors into their active form, which subsequently promotes transcription of Gli target genes[ 1 ]. (plos.org)
  • ATF 4 is a transcription factor, which means it tells the body to activate or regulate certain genes. (lifeboat.com)
  • The term was coined in 2012 by studies identifying several genes responsible for ferroptosis, including those associated with amino acids such as glutamate and cysteine, and lipid metabolism [ 4 - 6 ]. (oncotarget.com)
  • Factor de transcripción activador que regula la expresión de diversos GENES implicados en el metabolismo y transporte de aminoácidos. (bvsalud.org)
  • These findings establish that phenolic antioxidants activate Mt1 transcription by a zinc-dependent mechanism, which involves MTF-1 binding to metal regulator elements in the Mt1 gene promoter. (cdc.gov)
  • 4) We will probe the biological (nutritional) function of carotenoid metabolites in multiple ways: (a) we will use cell lines that we have shown have characteristic functional responses to treatment with dietary carotenoids and ask whether these responses are obtained by direct treatment with the cleavage products and (b) we will ask whether these cleavage products and metabolites directly activate or antagonize ligand-dependent transcription factors. (nih.gov)
  • Induction of metallothionein l by phenolic antioxidants requires metal-activated transcription factor 1 (MTF-1) and zinc. (cdc.gov)
  • On the contrary, HNE did not stimulate nuclear translocation of NF-kappa B. The diverging effect of HNE on the two transcription factors is likely related to the demonstrated differential activation pathway of AP-1 and NF-kappa B in macrophages. (unito.it)
  • In the second maturation phase, the first morphologically recognizable cell, the pro-erythroblast undergoes cytoplasmic and nuclear alterations through 4 or 5 mitotic divisions resulting in basophilic, polychromatophilic and orthochromatic normoblasts. (nih.gov)
  • The Th2 transcription factor c-Maf inhibits IL-12p35 gene expression in activated macrophages by targeting NF-kappaB nuclear translocation. (cornell.edu)
  • Exposed cells also demonstrated an increase in the activation of the transcription activating factor Nuclear-Factor-kappa-B (NF-kB). (cdc.gov)
  • The purpose of this research was to investigate whether asbestos (1332214) induces an active endothelial cell phenotype, resulting in the increased expression of growth factors and proteases, which are relevant to the development of fibrosis. (cdc.gov)
  • In parallel, the produced kynurenine activates the aryl-hydrocarbon receptor (AhR) ( 7 , 8 ). (spandidos-publications.com)
  • While distinct molecularly, these different axes are likely mutually beneficial and activated in parallel. (biomedcentral.com)
  • Following release of suppression, SMO translocates from endosomes to the primary cilium where its extracellular cysteine-rich domain (CRD) becomes exposed to a yet unknown natural ligand, proposed to be cholesterol[ 4 ]. (plos.org)
  • Human pancreatic cancer PANC-1 and BxPC-3 and human colorectal cancer HCT116 cells were treated with ferroptotic agents such as erastin and artesunate (ART) in combination with the apoptotic agent tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (oncotarget.com)
  • 4. Tumor-specific MHC-II expression drives a unique pattern of resistance to immunotherapy via LAG-3/FCRL6 engagement. (nih.gov)
  • The mechanisms responsible for the increased adipos- of Patient with ity are changes in gene expression of multiple enzymes and transcription factors by the virus ( 8-15 ). (cdc.gov)
  • In conjunction with these seemingly beneficial effects, VIVIT treatment elicited a marked increase in the expression of the prosynaptogenic factor SPARCL1 (hevin), especially in hippocampal tissue ipsilateral to the CCI injury. (jneurosci.org)
  • 13. Single-Cell RNA Sequencing of Tumor-Infiltrating NK Cells Reveals that Inhibition of Transcription Factor HIF-1α Unleashes NK Cell Activity. (nih.gov)
  • alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin 18 (IL-18), and tumor necrosis factor- a (TNF- a ) levels in rat serum were also analyzed using ELISA kits. (fluoridealert.org)
  • Moreover, we revealed that ERS alleviator (4-PBA) could induce proliferation and prevent ERS and apoptosis in fluorine-exposed AML12 cells. (fluoridealert.org)
  • Histone deacetylase (HDAC) can modify chromatin structure and regulate transcription factor activity [ 15 ]. (fluoridealert.org)
  • Epigenetic mechanisms, especially methylations on histone H3 lysine 4 (H3K4), H3K9 and H3K27, have also been implicated in regulating adipogenesis and adipocyte functions. (nih.gov)
  • 2022 Apr 1;152(4):926-938. (nih.gov)
  • tibodies to Adv 36 and obesity ( 4-8 ). (cdc.gov)
  • terol and triglyceride levels were paradoxically reduced, Hypothyroidism, chemoradiation-induced hypogonadism, despite the obesity ( 1-4 ). (cdc.gov)
  • Biogenic 4-hydroxy-2-nonenal activates transcription factor AP-1 but not NF-kappa B in cells of the macrophage lineage. (unito.it)
  • The cells respond to both chrysotile (12001295) and crocidolite (12001284) asbestos fibers by changing cell morphology in focal areas of fiber contact, assuming a spindled appearance, indicative of the activated endothelial cell. (cdc.gov)
  • While long-term exposure to fluoride in the air, food, and water can lead to fluorosis, it can also cause dental fluorosis and fluorosis bone disease [ 4 ]. (fluoridealert.org)
  • 6. Activating transcription factor 4 is translationally regulated by hypoxic stress. (nih.gov)
  • Using a controlled cortical impact (CCI) procedure in rats, we show that traumatic brain injury is associated with an increase in the activities of NFATs 1 and 4 in the hippocampus at 7 d after injury. (jneurosci.org)
  • Hh signaling is cilia-independent and requires the kinesin Costal2 (4) (Kif7/27 in vertebrates) and the kinase Fused (5). (bioskinrevive.com)
  • I ly region 4 gene was transferred to a retrovirus and inserted nfection with human adenovirus 36 (Adv 36) has been into preadipocytes in vitro, the gene was capable of induc- reported to cause a large accumulation of fat in 4 animals ing the enzymes and enhancing fat accumulation ( 13 ). (cdc.gov)
  • Development of the Adv 36 open reading frame 1 early region 4 gene and of massive lipomatosis may be caused by Adv 36. (cdc.gov)
  • This will be accomplished by quantitation of the immediate post- prandial plasma concentrations of parent carotenoids and metabolites after subjects consume a single serving of tomato juice containing nutritionally relevant amounts of beta-carotene or lycopene as well as by quantitation of steady state concentrations in plasma after 4 weeks of daily consumption. (nih.gov)

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