An integrin found in FIBROBLASTS; PLATELETS; MONOCYTES, and LYMPHOCYTES. Integrin alpha5beta1 is the classical receptor for FIBRONECTIN, but it also functions as a receptor for LAMININ and several other EXTRACELLULAR MATRIX PROTEINS.
This integrin alpha subunit combines with INTEGRIN BETA1 to form a receptor (INTEGRIN ALPHA5BETA1) that binds FIBRONECTIN and LAMININ. It undergoes posttranslational cleavage into a heavy and a light chain that are connected by disulfide bonds.
An integrin alpha subunit that primarily combines with INTEGRIN BETA1 to form the INTEGRIN ALPHA2BETA1 heterodimer. It contains a domain which has homology to collagen-binding domains found in von Willebrand factor.
Cell surface receptor for LAMININ, epiligrin, FIBRONECTINS, entactin, and COLLAGEN. Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT MEMBRANE as well as in cell migration, and may regulate the functions of other integrins. Two alternatively spliced isoforms of the alpha subunit (INTEGRIN ALPHA3), are differentially expressed in different cell types.
An integrin found on fibroblasts, platelets, endothelial and epithelial cells, and lymphocytes where it functions as a receptor for COLLAGEN and LAMININ. Although originally referred to as the collagen receptor, it is one of several receptors for collagen. Ligand binding to integrin alpha2beta1 triggers a cascade of intracellular signaling, including activation of p38 MAP kinase.
An integrin alpha subunit that primarily associates with INTEGRIN BETA1 or INTEGRIN BETA4 to form laminin-binding heterodimers. Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their cytoplasmic domains and are regulated in a tissue-specific and developmental stage-specific manner.
Integrin alpha1beta1 functions as a receptor for LAMININ and COLLAGEN. It is widely expressed during development, but in the adult is the predominant laminin receptor (RECEPTORS, LAMININ) in mature SMOOTH MUSCLE CELLS, where it is important for maintenance of the differentiated phenotype of these cells. Integrin alpha1beta1 is also found in LYMPHOCYTES and microvascular endothelial cells, and may play a role in angiogenesis. In SCHWANN CELLS and neural crest cells, it is involved in cell migration. Integrin alpha1beta1 is also known as VLA-1 and CD49a-CD29.
A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.
An integrin alpha subunit that occurs as alternatively spliced isoforms. The isoforms are differentially expressed in specific cell types and at specific developmental stages. Integrin alpha3 combines with INTEGRIN BETA1 to form INTEGRIN ALPHA3BETA1 which is a heterodimer found primarily in epithelial cells.
The alpha subunits of integrin heterodimers (INTEGRINS), which mediate ligand specificity. There are approximately 18 different alpha chains, exhibiting great sequence diversity; several chains are also spliced into alternative isoforms. They possess a long extracellular portion (1200 amino acids) containing a MIDAS (metal ion-dependent adhesion site) motif, and seven 60-amino acid tandem repeats, the last 4 of which form EF HAND MOTIFS. The intracellular portion is short with the exception of INTEGRIN ALPHA4.
This intrgrin is a key component of HEMIDESMOSOMES and is required for their formation and maintenance in epithelial cells. Integrin alpha6beta4 is also found on thymocytes, fibroblasts, and Schwann cells, where it functions as a laminin receptor (RECEPTORS, LAMININ) and is involved in wound healing, cell migration, and tumor invasiveness.
An integrin alpha subunit that binds COLLAGEN and LAMININ though its I domain. It combines with INTEGRIN BETA1 to form the heterodimer INTEGRIN ALPHA1BETA1.
A cell surface receptor mediating cell adhesion to the EXTRACELLULAR MATRIX and to other cells via binding to LAMININ. It is involved in cell migration, embryonic development, leukocyte activation and tumor cell invasiveness. Integrin alpha6beta1 is the major laminin receptor on PLATELETS; LEUKOCYTES; and many EPITHELIAL CELLS, and ligand binding may activate a number of signal transduction pathways. Alternative splicing of the cytoplasmic domain of the alpha6 subunit (INTEGRIN ALPHA6) results in the formation of A and B isoforms of the heterodimer, which are expressed in a tissue-specific manner.
An integrin that binds to a variety of plasma and extracellular matrix proteins containing the conserved RGD amino acid sequence and modulates cell adhesion. Integrin alphavbeta3 is highly expressed in OSTEOCLASTS where it may play role in BONE RESORPTION. It is also abundant in vascular smooth muscle and endothelial cells, and in some tumor cells, where it is involved in angiogenesis and cell migration. Although often referred to as the vitronectin receptor there is more than one receptor for vitronectin (RECEPTORS, VITRONECTIN).
An integrin alpha subunit that is unique in that it does not contain an I domain, and its proteolytic cleavage site is near the middle of the extracellular portion of the polypeptide rather than close to the membrane as in other integrin alpha subunits.
An integrin beta subunit of approximately 85-kDa in size which has been found in INTEGRIN ALPHAIIB-containing and INTEGRIN ALPHAV-containing heterodimers. Integrin beta3 occurs as three alternatively spliced isoforms, designated beta3A-C.
Adherence of cells to surfaces or to other cells.
Integrin beta chains combine with integrin alpha chains to form heterodimeric cell surface receptors. Integrins have traditionally been classified into functional groups based on the identity of one of three beta chains present in the heterodimer. The beta chain is necessary and sufficient for integrin-dependent signaling. Its short cytoplasmic tail contains sequences critical for inside-out signaling.
An alpha integrin with a molecular weight of 160-kDa that is found in a variety of cell types. It undergoes posttranslational cleavage into a heavy and a light chain that are connected by disulfide bonds. Integrin alphaV can combine with several different beta subunits to form heterodimers that generally bind to RGD sequence-containing extracellular matrix proteins.
Integrin alpha4beta1 is a FIBRONECTIN and VCAM-1 receptor present on LYMPHOCYTES; MONOCYTES; EOSINOPHILS; NK CELLS and thymocytes. It is involved in both cell-cell and cell- EXTRACELLULAR MATRIX adhesion and plays a role in INFLAMMATION, hematopoietic cell homing and immune function, and has been implicated in skeletal MYOGENESIS; NEURAL CREST migration and proliferation, lymphocyte maturation and morphogenesis of the PLACENTA and HEART.
Also known as CD104 antigen, this protein is distinguished from other beta integrins by its relatively long cytoplasmic domain (approximately 1000 amino acids vs. approximately 50). Five alternatively spliced isoforms have been described.
Receptors such as INTEGRIN ALPHAVBETA3 that bind VITRONECTIN with high affinity and play a role in cell migration. They also bind FIBRINOGEN; VON WILLEBRAND FACTOR; osteopontin; and THROMBOSPONDINS.
Integrin beta-1 chains which are expressed as heterodimers that are noncovalently associated with specific alpha-chains of the CD49 family (CD49a-f). CD29 is expressed on resting and activated leukocytes and is a marker for all of the very late activation antigens on cells. (from: Barclay et al., The Leukocyte Antigen FactsBook, 1993, p164)
Collagen receptors are cell surface receptors that modulate signal transduction between cells and the EXTRACELLULAR MATRIX. They are found in many cell types and are involved in the maintenance and regulation of cell shape and behavior, including PLATELET ACTIVATION and aggregation, through many different signaling pathways and differences in their affinities for collagen isoforms. Collagen receptors include discoidin domain receptors, INTEGRINS, and glycoprotein VI.
Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.
Specific cell surface receptors which bind to FIBRONECTINS. Studies have shown that these receptors function in certain types of adhesive contact as well as playing a major role in matrix assembly. These receptors include the traditional fibronectin receptor, also called INTEGRIN ALPHA5BETA1 and several other integrins.
Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. It is an integrin complex containing INTEGRIN ALPHAIIB and INTEGRIN BETA3 which recognizes the arginine-glycine-aspartic acid (RGD) sequence present on several adhesive proteins. As such, it is a receptor for FIBRINOGEN; VON WILLEBRAND FACTOR; FIBRONECTIN; VITRONECTIN; and THROMBOSPONDINS. A deficiency of GPIIb-IIIa results in GLANZMANN THROMBASTHENIA.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
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.
Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
Peptides composed of between two and twelve amino acids.
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 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.
A blood plasma glycoprotein that mediates cell adhesion and interacts with proteins of the complement, coagulation, and fibrinolytic cascade. (From Segen, Dictionary of Modern Medicine, 1992)
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 polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.
Tetraspanin proteins found associated with LAMININ-binding INTEGRINS. The CD151 antigens may play a role in the regulation of CELL MOTILITY.
Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.
A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
Glycoprotein molecules on the surface of cells that react with or bind to laminin whose function allows the binding of epithelial cells to the basement membrane. The molecular weight of this high-affinity receptor is 67 kD.
A 235-kDa cytoplasmic protein that is also found in platelets. It has been localized to regions of cell-substrate adhesion. It binds to INTEGRINS; VINCULIN; and ACTINS and appears to participate in generating a transmembrane connection between the extracellular matrix and the cytoskeleton.
Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
Antibodies produced by a single clone of cells.
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.
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.
A group of INTEGRINS that includes the platelet outer membrane glycoprotein GPIIb-IIIa (PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX) and the vitronectin receptor (RECEPTORS, VITRONECTIN). They play a major role in cell adhesion and serve as receptors for fibronectin, von Willebrand factor, and vitronectin.
A family of non-receptor, PROLINE-rich protein-tyrosine kinases.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.
Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.
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 cell line derived from cultured tumor cells.
Established cell cultures that have the potential to propagate indefinitely.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
Proteins prepared by recombinant DNA technology.
A non-receptor protein tyrosine kinase that is localized to FOCAL ADHESIONS and is a central component of integrin-mediated SIGNAL TRANSDUCTION PATHWAYS. Focal adhesion kinase 1 interacts with PAXILLIN and undergoes PHOSPHORYLATION in response to adhesion of cell surface integrins to the EXTRACELLULAR MATRIX. Phosphorylated p125FAK protein binds to a variety of SH2 DOMAIN and SH3 DOMAIN containing proteins and helps regulate CELL ADHESION and CELL MIGRATION.
Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
An anchoring junction of the cell to a non-cellular substrate, similar in morphology to halves of DESMOSOMES. They are composed of specialized areas of the plasma membrane where INTERMEDIATE FILAMENTS bind on the cytoplasmic face to the transmembrane linkers, INTEGRINS, via intracellular attachment proteins, while the extracellular domain of the integrins binds to EXTRACELLULAR MATRIX PROTEINS.
A congenital bleeding disorder with prolonged bleeding time, absence of aggregation of platelets in response to most agents, especially ADP, and impaired or absent clot retraction. Platelet membranes are deficient in or have a defect in the glycoprotein IIb-IIIa complex (PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX).
Retraction of a clot resulting from contraction of PLATELET pseudopods attached to FIBRIN strands. The retraction is dependent on the contractile protein thrombosthenin. Clot retraction is used as a measure of platelet function.
A series of progressive, overlapping events, triggered by exposure of the PLATELETS to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
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.
Paxillin is a signal transducing adaptor protein that localizes to FOCAL ADHESIONS via its four LIM domains. It undergoes PHOSPHORYLATION in response to integrin-mediated CELL ADHESION, and interacts with a variety of proteins including VINCULIN; FOCAL ADHESION KINASE; PROTO-ONCOGENE PROTEIN PP60(C-SRC); and PROTO-ONCOGENE PROTEIN C-CRK.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
Platelet membrane glycoprotein IIb is an integrin alpha subunit that heterodimerizes with INTEGRIN BETA3 to form PLATELET GLYCOPROTEIN GPIIB-IIIA COMPLEX. It is synthesized as a single polypeptide chain which is then postranslationally cleaved and processed into two disulfide-linked subunits of approximately 18 and 110 kDa in size.
A subtype of tetraspanin proteins that play a role in cell adhesion, cell motility, and tumor metastasis. CD9 antigens take part in the process of platelet activation and aggregation, the formation of paranodal junctions in neuronal tissue, and the fusion of sperm with egg.
A non-fibrillar collagen found in the structure of BASEMENT MEMBRANE. Collagen type IV molecules assemble to form a sheet-like network which is involved in maintaining the structural integrity of basement membranes. The predominant form of the protein is comprised of two alpha1(IV) subunits and one alpha2(IV) subunit, however, at least six different alpha subunits can be incorporated into the heterotrimer.
A major adhesion-associated heterodimer molecule expressed by MONOCYTES; GRANULOCYTES; NK CELLS; and some LYMPHOCYTES. The alpha subunit is the CD11C ANTIGEN, a surface antigen expressed on some myeloid cells. The beta subunit is the CD18 ANTIGEN.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Members of the integrin family appearing late after T-cell activation. They are a family of proteins initially identified at the surface of stimulated T-cells, but now identified on a variety of cell types. At least six VLA antigens have been identified as heterodimeric adhesion receptors consisting of a single common beta-subunit and different alpha-subunits.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., COLLAGEN; ELASTIN; FIBRONECTINS; and LAMININ).
The part of a cell that contains the CYTOSOL and small structures excluding the CELL NUCLEUS; MITOCHONDRIA; and large VACUOLES. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
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.
A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.
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.
An anchoring junction of the cell to a non-cellular substrate. It is composed of a specialized area of the plasma membrane where bundles of the ACTIN CYTOSKELETON terminate and attach to the transmembrane linkers, INTEGRINS, which in turn attach through their extracellular domains to EXTRACELLULAR MATRIX PROTEINS.
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)
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.
The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm.
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.
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.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Single chains of amino acids that are the units of multimeric PROTEINS. Multimeric proteins can be composed of identical or non-identical subunits. One or more monomeric subunits may compose a protomer which itself is a subunit structure of a larger assembly.
The rate dynamics in chemical or physical systems.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
An integrin heterodimer widely expressed on cells of hematopoietic origin. CD11A ANTIGEN comprises the alpha chain and the CD18 antigen (ANTIGENS, CD18) the beta chain. Lymphocyte function-associated antigen-1 is a major receptor of T-CELLS; B-CELLS; and GRANULOCYTES. It mediates the leukocyte adhesion reactions underlying cytolytic conjugate formation, helper T-cell interactions, and antibody-dependent killing by NATURAL KILLER CELLS and granulocytes. Intracellular adhesion molecule-1 has been defined as a ligand for lymphocyte function-associated antigen-1.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Cell surface glycoproteins on lymphocytes and other leukocytes that mediate adhesion to specialized blood vessels called high endothelial venules. Several different classes of lymphocyte homing receptors have been identified, and they appear to target different surface molecules (addressins) on high endothelial venules in different tissues. The adhesion plays a crucial role in the trafficking of lymphocytes.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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.
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.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
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.
A family of polypeptides purified from snake venoms, which contain the arginine-glycine-aspartic acid (RGD) sequence. The RGD tripeptide binds to integrin receptors and thus competitively inhibits normal integrin-ligand interactions. Disintegrins thus block adhesive functions and act as platelet aggregation inhibitors.
Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
A PROTEIN-TYROSINE KINASE family that was originally identified by homology to the Rous sarcoma virus ONCOGENE PROTEIN PP60(V-SRC). They interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways. Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes.
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.
A CCN protein family member that regulates a variety of extracellular functions including CELL ADHESION; CELL MIGRATION; and EXTRACELLULAR MATRIX synthesis. It may play an important role in the development of branched CAPILLARIES during EMBRYOGENESIS.
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.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A darkly stained mat-like EXTRACELLULAR MATRIX (ECM) that separates cell layers, such as EPITHELIUM from ENDOTHELIUM or a layer of CONNECTIVE TISSUE. The ECM layer that supports an overlying EPITHELIUM or ENDOTHELIUM is called basal lamina. Basement membrane (BM) can be formed by the fusion of either two adjacent basal laminae or a basal lamina with an adjacent reticular lamina of connective tissue. BM, composed mainly of TYPE IV COLLAGEN; glycoprotein LAMININ; and PROTEOGLYCAN, provides barriers as well as channels between interacting cell layers.
The most common form of fibrillar collagen. It is a major constituent of bone (BONE AND BONES) and SKIN and consists of a heterotrimer of two alpha1(I) and one alpha2(I) chains.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Compounds and molecular complexes that consist of very large numbers of atoms and are generally over 500 kDa in size. In biological systems macromolecular substances usually can be visualized using ELECTRON MICROSCOPY and are distinguished from ORGANELLES by the lack of a membrane structure.
Conjugated proteins in which mucopolysaccharides are combined with proteins. The mucopolysaccharide moiety is the predominant group with the protein making up only a small percentage of the total weight.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
A negatively-charged extracellular matrix protein that plays a role in the regulation of BONE metabolism and a variety of other biological functions. Cell signaling by osteopontin may occur through a cell adhesion sequence that recognizes INTEGRIN ALPHA-V BETA-3.
Serologic tests in which a positive reaction manifested by visible CHEMICAL PRECIPITATION occurs when a soluble ANTIGEN reacts with its precipitins, i.e., ANTIBODIES that can form a precipitate.
An interleukin-1 subtype that occurs as a membrane-bound pro-protein form that is cleaved by proteases to form a secreted mature form. Unlike INTERLEUKIN-1BETA both membrane-bound and secreted forms of interleukin-1alpha are biologically active.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
Platelet membrane glycoprotein complex essential for normal platelet adhesion and clot formation at sites of vascular injury. It is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX. Glycoprotein Ib functions as a receptor for von Willebrand factor and for thrombin. Congenital deficiency of the GPIb-IX complex results in Bernard-Soulier syndrome. The platelet glycoprotein GPV associates with GPIb-IX and is also absent in Bernard-Soulier syndrome.
The aggregation of soluble ANTIGENS with ANTIBODIES, alone or with antibody binding factors such as ANTI-ANTIBODIES or STAPHYLOCOCCAL PROTEIN A, into complexes large enough to fall out of solution.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
A cytoskeletal linker protein with a molecular weight of greater than 500 kDa. It binds INTERMEDIATE FILAMENTS; MICROTUBULES; and ACTIN CYTOSKELETON and plays a central role in the organization and stability of the CYTOSKELETON. Plectin is phosphorylated by CALMODULIN KINASE; PROTEIN KINASE A; and PROTEIN KINASE C.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Elements of limited time intervals, contributing to particular results or situations.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
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.
Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
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.
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
The process by which two molecules of the same chemical composition form a condensation product or polymer.
Glycoproteins found on the membrane or surface of cells.
A genus of the family Muridae consisting of eleven species. C. migratorius, the grey or Armenian hamster, and C. griseus, the Chinese hamster, are the two species used in biomedical research.
A dynamic actin-rich extension of the surface of an animal cell used for locomotion or prehension of food.
Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible.
A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
A rac GTP-binding protein involved in regulating actin filaments at the plasma membrane. It controls the development of filopodia and lamellipodia in cells and thereby influences cellular motility and adhesion. It is also involved in activation of NADPH OXIDASE. This enzyme was formerly listed as EC 3.6.1.47.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Rare autosomal recessive congenital malformation syndrome characterized by cryptophthalmos, SYNDACTYLY and UROGENITAL ABNORMALITIES. Other anomalies of bone, ear, lung, and nose are common. Mutations on FRAS1 and FREM2 are associated with the syndrome.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.
Hexameric extracellular matrix glycoprotein transiently expressed in many developing organs and often re-expressed in tumors. It is present in the central and peripheral nervous systems as well as in smooth muscle and tendons. (From Kreis & Vale, Guidebook to the Extracellular Matrix and Adhesion Proteins, 1993, p93)
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
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.
Brain waves characterized by a relatively high voltage or amplitude and a frequency of 8-13 Hz. They constitute the majority of waves recorded by EEG registering the activity of the parietal and occipital lobes when the individual is awake, but relaxed with the eyes closed.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Venoms from SNAKES of the viperid family. They tend to be less toxic than elapid or hydrophid venoms and act mainly on the vascular system, interfering with coagulation and capillary membrane integrity and are highly cytotoxic. They contain large amounts of several enzymes, other factors, and some toxins.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Positively charged atoms, radicals or groups of atoms with a valence of plus 2, which travel to the cathode or negative pole during electrolysis.
Venoms from snakes of the subfamily Crotalinae or pit vipers, found mostly in the Americas. They include the rattlesnake, cottonmouth, fer-de-lance, bushmaster, and American copperhead. Their venoms contain nontoxic proteins, cardio-, hemo-, cyto-, and neurotoxins, and many enzymes, especially phospholipases A. Many of the toxins have been characterized.
A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A high-molecular-weight plasma protein, produced by endothelial cells and megakaryocytes, that is part of the factor VIII/von Willebrand factor complex. The von Willebrand factor has receptors for collagen, platelets, and ristocetin activity as well as the immunologically distinct antigenic determinants. It functions in adhesion of platelets to collagen and hemostatic plug formation. The prolonged bleeding time in VON WILLEBRAND DISEASES is due to the deficiency of this factor.
A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035)
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Transport proteins that carry specific substances in the blood or across cell membranes.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A genetically related subfamily of RAP GTP-BINDING PROTEINS that share homology with RAS PROTEINS. They bind to Ras effectors but do not activate them, therefore they may antagonize the effects of RAS PROTEINS. This enzyme was formerly listed as EC 3.6.1.47.
Calcium-dependent cell adhesion proteins. They are important in the formation of ADHERENS JUNCTIONS between cells. Cadherins are classified by their distinct immunological and tissue specificities, either by letters (E- for epithelial, N- for neural, and P- for placental cadherins) or by numbers (cadherin-12 or N-cadherin 2 for brain-cadherin). Cadherins promote cell adhesion via a homophilic mechanism as in the construction of tissues and of the whole animal body.
Deficiency of the protease inhibitor ALPHA 1-ANTITRYPSIN that manifests primarily as PULMONARY EMPHYSEMA and LIVER CIRRHOSIS.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
Unstable isotopes of copper that decay or disintegrate emitting radiation. Cu atoms with atomic weights 58-62, 64, and 66-68 are radioactive copper isotopes.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.
Drugs that selectively bind to and activate alpha adrenergic receptors.
A mitogen-activated protein kinase subfamily that is widely expressed and plays a role in regulation of MEIOSIS; MITOSIS; and post mitotic functions in differentiated cells. The extracellular signal regulated MAP kinases are regulated by a broad variety of CELL SURFACE RECEPTORS and can be activated by certain CARCINOGENS.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.

Quantitative changes in integrin and focal adhesion signaling regulate myoblast cell cycle withdrawal. (1/284)

We previously demonstrated contrasting roles for integrin alpha subunits and their cytoplasmic domains in controlling cell cycle withdrawal and the onset of terminal differentiation (Sastry, S., M. Lakonishok, D. Thomas, J. Muschler, and A.F. Horwitz. 1996. J. Cell Biol. 133:169-184). Ectopic expression of the integrin alpha5 or alpha6A subunit in primary quail myoblasts either decreases or enhances the probability of cell cycle withdrawal, respectively. In this study, we addressed the mechanisms by which changes in integrin alpha subunit ratios regulate this decision. Ectopic expression of truncated alpha5 or alpha6A indicate that the alpha5 cytoplasmic domain is permissive for the proliferative pathway whereas the COOH-terminal 11 amino acids of alpha6A cytoplasmic domain inhibit proliferation and promote differentiation. The alpha5 and alpha6A cytoplasmic domains do not appear to initiate these signals directly, but instead regulate beta1 signaling. Ectopically expressed IL2R-alpha5 or IL2R-alpha6A have no detectable effect on the myoblast phenotype. However, ectopic expression of the beta1A integrin subunit or IL2R-beta1A, autonomously inhibits differentiation and maintains a proliferative state. Perturbing alpha5 or alpha6A ratios also significantly affects activation of beta1 integrin signaling pathways. Ectopic alpha5 expression enhances expression and activation of paxillin as well as mitogen-activated protein (MAP) kinase with little effect on focal adhesion kinase (FAK). In contrast, ectopic alpha6A expression suppresses FAK and MAP kinase activation with a lesser effect on paxillin. Ectopic expression of wild-type and mutant forms of FAK, paxillin, and MAP/erk kinase (MEK) confirm these correlations. These data demonstrate that (a) proliferative signaling (i.e., inhibition of cell cycle withdrawal and the onset of terminal differentiation) occurs through the beta1A subunit and is modulated by the alpha subunit cytoplasmic domains; (b) perturbing alpha subunit ratios alters paxillin expression and phosphorylation and FAK and MAP kinase activation; (c) quantitative changes in the level of adhesive signaling through integrins and focal adhesion components regulate the decision of myoblasts to withdraw from the cell cycle, in part via MAP kinase.  (+info)

Extracellular matrix regulates apoptosis in mammary epithelium through a control on insulin signaling. (2/284)

Adherent epithelial cells require interactions with the extracellular matrix for their survival, though the mechanism is ill-defined. In long term cultures of primary mammary epithelial cells, a laminin-rich basement membrane (BM) but not collagen I suppresses apoptosis, indicating that adhesion survival signals are specific in their response (. J. Cell Sci. 109:631-642). We now demonstrate that the signal from BM is mediated by integrins and requires both the alpha6 and beta1 subunits. In addition, a hormonal signal from insulin or insulin-like growth factors, but not hydrocortisone or prolactin, is necessary to suppress mammary cell apoptosis, indicating that BM and soluble factors cooperate in survival signaling. Insulin induced autophosphorylation of its receptor whether mammary cells were cultured on collagen I or BM substrata. However, both the tyrosine phosphorylation of insulin receptor substrate-1 and its association with phosphatidylinositol 3-kinase were enhanced in cells cultured on BM, as was the phosphorylation of the phosphatidylinositol 3-kinase effector, protein kinase B. These results suggest a novel extracellular matrix-dependent restriction point in insulin signaling in mammary epithelial cells. The proximal signal transduction event of insulin receptor phosphorylation is not dependent on extracellular matrix, but the activation of downstream effectors requires adhesion to BM. Since phosphatidylinositol 3-kinase was required for mammary epithelial cell survival, we propose that a possible mechanism for BM-mediated suppression of apoptosis is through its facilitative effects on insulin signaling.  (+info)

beta1- and alpha6-integrin are surface markers on mouse spermatogonial stem cells. (3/284)

Although spermatogenesis is essential for reproduction, little is known about spermatogonial stem cells. These cells provide the basis for spermatogenesis throughout adult life by undergoing self-renewal and by providing progeny that differentiate into spermatozoa. A major impediment to our understanding of the biology of these stem cells is the inability to distinguish them from spermatogonia that are committed to differentiation. We made use of the known association of stem cells with basement membranes and our spermatogonial transplantation assay system to identify specific molecular markers on the stem cell surface. Selection of mouse testis cells with anti-beta1- or anti-alpha6-integrin antibody, but not anti-c-kit antibody, produced cell populations with a significantly enhanced ability to colonize recipient testes and generate donor cell-derived spermatogenesis. We demonstrate spermatogonial stem cell-associated antigens by using an assay system based on biological function. Furthermore, the presence of surface integrins on spermatogonial stem cells suggests that these cells share elements of a common molecular machinery with stem cells in other tissues.  (+info)

alpha6 Integrin is regulated with lens cell differentiation by linkage to the cytoskeleton and isoform switching. (4/284)

The developing chicken embryo lens provides a unique model for examining the relationship between alpha6 integrin expression and cell differentiation, since multiple stages of differentiation are expressed concurrently at one stage of development. We demonstrate that alpha6 integrin is likely to mediate the inductive effects of laminin on lens differentiation as well as to function in a matrix-independent manner along the cell-cell interfaces of the differentiating cortical lens fiber cells. Both alpha6 isoform expression and its linkage to the cytoskeleton were regulated in a differentiation-specific manner. The association of alpha6 integrin with the Triton-insoluble cytoskeleton increased as the lens cells differentiated, reaching its highest levels in the cortical fiber region where the lens fiber cells are formed. In this region of the lens alpha6 integrin was uniquely localized along the cell-cell borders of the differentiating fiber cells, similar to beta1. alpha6beta4, the primary transmembrane protein of hemidesmosomes, is also expressed in the lens, but in the absence of hemidesmosomes. Differential expression of alpha6A and alpha6B isoforms with lens cell differentiation was seen at both the mRNA and the protein levels. RT-PCR studies demonstrated that alpha6B was the predominant isoform expressed both early in development, embryonic day 4, and in the epithelial regions of the day 10 embryonic lens. Isoform switching, with alpha6A now the predominant isoform, occurred in the fiber cell zones. Immunoprecipitation studies showed that alpha6B, which is characteristic of undifferentiated cells, was expressed by the lens epithelial cells but was dramatically reduced in the lens fiber zones. Expression of alpha6B began to drop as the cells initiated their differentiation and then dropped precipitously in the cortical fiber zone. In contrast, expression of the alpha6A isoform remained high until the cells became terminally differentiated. alpha6A was the predominant isoform expressed in the cortical fiber region. The down-regulation of alpha6B relative to alpha6A provides a developmental switch in the process of lens fiber cell differentiation.  (+info)

Synergistic activities of alpha3 and alpha6 integrins are required during apical ectodermal ridge formation and organogenesis in the mouse. (5/284)

Integrins alpha6beta1 and alpha6beta4 are cell surface receptors for laminins. Integrin alpha6-null mice die at birth with severe skin blistering and defects in the cerebral cortex and in the retina. Integrin alpha3beta1 can associate with laminins and other ligands. Integrin alpha3-null mice also die at birth, with kidney and lung defects at late stages of development, and moderate skin blistering. To investigate possible overlapping functions between alpha3 and alpha6 integrins, we analyzed the phenotype of compound alpha3-/-/alpha6-/- mutant embryos. Double homozygous mutant embryos were growth-retarded and displayed several developmental defects not observed in the single mutant animals. First, limb abnormalities characterized by an absence of digit separation and the fusion of preskeletal elements were observed. Further analyses indicated a defect in the apical ectodermal ridge, an essential limb organizing center. In the double mutant, the ridge appeared flattened, and ridge cells did not show a columnar morphology. A strong reduction in ridge cell proliferation and alterations of the basal lamina underlying the ectoderm were observed. These results suggest that alpha3 and alpha6 integrins are required for the organization or compaction of presumptive apical ectodermal ridge cells into a distinct differentiated structure. Additional defects were present: an absence of neural tube closure, bilateral lung hypoplasia, and several abnormalities in the urogenital tract. Finally, an aggravation of brain and eye lamination defects was observed. The presence of novel phenotypes in double mutant embryos demonstrates the synergism between alpha3 and alpha6 integrins and their essential roles in multiple processes during embryogenesis.  (+info)

Expression of the alpha6 integrin confers papillomavirus binding upon receptor-negative B-cells. (6/284)

Papillomaviruses (PV) bind to a wide range of cell lines in a specific and saturable manner. We have recently identified a candidate receptor for papillomavirus as the alpha6 integrin (Evander et al., J. Virol. 71, 2449-2456, 1997). We have further investigated the role the alpha6 integrin plays in PV binding. Here we show that the cells expressing the alpha6 integrin, partnered with either the beta4 integrin or the beta1 integrin, are equally able to bind PV HPV6b L1 virus-like particles, indicating that the beta partner does not play a major role in virus binding. In order to provide definitive evidence that the alpha6 integrin is required for PV binding we undertook to genetically complement the receptor-negative B-cell line DG75 by expressing the human alpha6A gene. The transduction of the alpha6 integrin gene into DG75 cells results in the cell surface expression of the alpha6 protein and this expression confers upon DG75 cells the ability to bind laminin, a normal ligand for alpha6 integrin. Furthermore, the alpha6 protein is partnered with the beta1 integrin in DG75 cells. Finally, we show that the DG75-alpha6 cells were able to bind papillomavirus VLPs and this binding was inhibited by a functionally blocking anti-alpha6 antibody. Together these data indicate that the alpha6 integrin is a primary cell receptor for papillomaviruses and is both necessary and sufficient for PV binding.  (+info)

Interleukin-10 receptors are expressed by basement membrane anchored, alpha(6) integrin(+) cytotrophoblast cells in early human placenta. (7/284)

Cytotrophoblast cells produce interleukin (IL)-10 and express IL-10 receptor mRNA in culture. Furthermore, IL-10 dramatically reduces the synthesis of matrix metalloproteinase (MMP)-9 and the invasivity of cytotrophoblast cells in vitro, suggesting that an autocrine regulatory role in vivo is also possible. To test this hypothesis we investigated the expression of IL-10 receptor protein by first trimester cytotrophoblasts both in vitro and in situ, using flow cytometry and immunohistochemistry. Flow cytometric analyses demonstrated that 75-80% of cytotrophoblasts are able to bind labelled IL-10, suggesting that these cells possess IL-10 receptors in vitro. Serial sections of early human placentae stained for either alpha(5) and alpha(6) integrin subunits, or for IL-10 receptors respectively, revealed that placental cytotrophoblasts possess cell surface IL-10 receptors not only in vitro, but also in vivo. IL-10 receptors were present mainly on alpha(6) integrin expressing villous cytotrophoblast cells and on alpha(6)-positive cells of invasive cell columns located nearest the villous stroma. Differentiated trophoblasts (i.e. alpha(5)-positive cells and villous syncytiotrophoblasts) showed no reactivity. This differential expression of IL-10 receptors suggests that IL-10 might suppress the invasivity of undifferentiated cytotrophoblast cells, in vivo, preserving their non-invasive state in an autocrine manner. The possible involvement in cytotrophoblast proliferation and/or differentiation is also discussed.  (+info)

Partial rescue of epithelial phenotype in integrin beta4 null mice by a keratin-5 promoter driven human integrin beta4 transgene. (8/284)

Integrin beta4 null mice exhibit extensive epidermal detachment, reminiscent of the human skin blistering disease junctional epidermolysis bullosa associated with pyloric atresia. Hemidesmosomes, the stable adhesion structures of squamous epithelia, are not formed in the absence of alpha6beta4. Null mutant mice die shortly after birth, but apart from their striking epithelial phenotype, no obvious developmental defects have been observed. To elucidate the cause of death in these mice, we generated transgenic mice with a heterologous construct consisting of the squamous epithelial-specific keratin-5 promoter and a human integrin beta4 subunit cDNA. The transgene was not expressed in the presence of endogenous beta4, probably as a result of competition for a limited pool of alpha6 subunits. In a beta4 null background, however, the transgene was expressed, and its expression pattern followed that of squamous epithelial-specific keratins. These rescued pups appeared healthy and ultrastructural analysis revealed that the interspecies heterodimer alpha6(mouse)/beta4(human) was sufficient to trigger the assembly of hemidesmosomes. After a variable period of up to 48 hours after birth these animals began to exhibit haemorrhages at the plantar and palmar areas. We observed the formation of small blisters and found that the transgene was not detectably expressed in this region, which is devoid of hair follicles. The rescued neonates became increasingly cyanotic and died soon after the onset of this phenomenon. We performed a developmental study of the expression of beta4 in the complete respiratory tract, but we found no correlation between the spatiotemporal distribution of beta4 and the onset of the respiratory insufficiency. It became clear, however, that there was a gradual detachment of squamous epithelia in the oral and nasal cavities which led to obstruction of the respiratory tract, suggesting that in beta4 null and rescued mice, neonatal death was a direct consequence of decreased adhesion properties of hairless squamous epithelia, rather than a developmental defect of the lungs.  (+info)

The term "thrombasthenia" comes from the Greek words "thrombos," meaning clot, and "basis," meaning foundation. It was first used by the British physician Sir William Osler in the late 19th century to describe a group of rare bleeding disorders characterized by abnormal platelet function.

There are three main types of thrombasthenia:

1. Bernard-Soulier syndrome: This is the most common type of thrombasthenia and is caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIb. People with this condition have large, fragile platelets that are prone to bleeding.
2. Glanzmann's thrombasthenia: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as platelet membrane glycoprotein (PMG) IIIa. People with this condition have small, irregular platelets that are unable to form proper blood clots.
3. Gray platelet syndrome: This is a rare type of thrombasthenia caused by a defect in the gene that codes for the protein known as alpha-granule membrane protein (AGM). People with this condition have small, gray-colored platelets that are prone to bleeding.

Thrombasthenia can be diagnosed through blood tests that evaluate platelet function and genetic testing to identify the specific defect responsible for the disorder. Treatment typically involves avoiding medications that can exacerbate bleeding, using platelet transfusions to increase platelet numbers, and in some cases, undergoing surgery to repair or remove affected blood vessels.

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.

1. Skin abnormalities: Fraser syndrome is associated with thin, fragile skin that may be covered with blisters or bullae. Individuals with this condition may have a higher risk of developing skin cancer.
2. Skeletal abnormalities: Fraser syndrome can cause defects in the development of bones, including short stature, bowed legs, and/or clubfoot.
3. Nervous system abnormalities: Individuals with Fraser syndrome may have neurological problems, such as seizures, developmental delays, and intellectual disability.
4. Eye abnormalities: Fraser syndrome can cause defects in the development of the eyes, including cataracts, glaucoma, and/or microphthalmia (small eyes).
5. Other abnormalities: Fraser syndrome can also cause a range of other abnormalities, such as heart defects, hearing loss, and/or dental problems.

Fraser syndrome is caused by mutations in the FRAS1 gene, which plays a critical role in the development of the skin, bones, and nervous system. The disorder is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by spontaneous mutations.

There is no cure for Fraser syndrome, and treatment is focused on managing the symptoms and preventing complications. This may include medication to control seizures, physical therapy to improve muscle strength and coordination, and surgery to correct skeletal deformities or other physical abnormalities.

Overall, Fraser syndrome is a rare and complex disorder that can affect multiple systems in the body. Early diagnosis and intervention are critical to managing the condition and improving outcomes for individuals with Fraser syndrome.

People with AATD have low levels of functional AAT in their blood, which can lead to premature lung disease and liver disease. The most common form of AATD is caused by the Pi*Z phenotype, which results from a missense mutation in the SERPINA1 gene. This mutation leads to misfolding and accumulation of AAT in the liver, where it is normally broken down and secreted into the bloodstream.

The most common symptoms of AATD are:

* Chronic obstructive pulmonary disease (COPD)
* Emphysema
* Lung fibrosis
* Liver cirrhosis
* Gallstones

The diagnosis of AATD is based on a combination of clinical symptoms, laboratory tests, and genetic analysis. Treatment for AATD typically involves managing the underlying symptoms and preventing complications. For example, individuals with COPD may receive bronchodilators and corticosteroids to help improve lung function and reduce inflammation. Liver disease may be treated with medications to slow the progression of cirrhosis or with liver transplantation in severe cases.

The goal of genetic counseling for AATD is to provide information about the risk of transmitting the disorder to offspring and to discuss options for prenatal testing and family planning. Prenatal testing can be performed on a fetus by analyzing a sample of cells from the placenta or amniotic fluid. Carrier testing can also be performed in individuals who have a family history of AATD.

The prognosis for AATD varies depending on the severity of the mutation and the specific symptoms present. With appropriate management, many individuals with AATD can lead active and productive lives. However, the disorder can be severe and life-threatening in some cases, especially if left untreated or if there is a delay in diagnosis.

Currently, there is no cure for AATD, and treatment is focused on managing symptoms and preventing complications. However, research into the genetics of AATD is ongoing, and new developments in gene therapy and other areas may provide hope for improved treatments and outcomes in the future.

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.

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.

There are several types of EB, classified based on the severity of symptoms and the age of onset. The most severe form, EB simplex, is the most common and affects approximately 1 in 20,000 to 1 in 50,000 births. Other forms of EB include junctional EB, dystrophic EB, and Kindler syndrome.

Symptoms of EB typically appear within the first few weeks of life and may include:

* Blisters and sores on the skin and mucous membranes
* Skin that is thin and fragile, with a characteristic "velvety" texture
* Delayed healing of wounds and scars
* Increased risk of infection
* Poor wound closure

Treatment for EB is focused on managing symptoms and preventing complications. This may include:

* Wound care and dressing changes
* Antibiotics to prevent infection
* Pain management
* Physical therapy to maintain joint mobility and prevent deformities
* Phototherapy to promote healing

There is currently no cure for EB, but researchers are working to develop new treatments and gene therapies to improve the lives of those affected by the condition. With proper management and support, however, many people with EB can lead active and fulfilling lives.

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.

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.

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.

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.

Symptoms of hereditary nephritis may include blood in the urine, proteinuria (excess protein in the urine), edema (swelling), high blood pressure, and kidney failure. The disorder can be diagnosed through blood tests, such as a viral load or genetic testing, and imaging studies, such as ultrasound or CT scans.

There is no cure for hereditary nephritis, but treatment options are available to manage the symptoms and slow the progression of the disease. Treatment may include medications to control blood pressure, reduce proteinuria, and prevent further kidney damage. In severe cases, dialysis or a kidney transplant may be necessary.

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.

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.

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.

Achlorhydria can be caused by various factors, such as:

1. Atrophic gastritis: This is a condition where the stomach lining becomes thin and inflamed, leading to a decrease in HCl production.
2. Autoimmune disorders: Conditions such as pernicious anemia and autoimmune gastritis can damage the stomach lining and lead to achlorhydria.
3. Medications: Certain medications, such as antacids and proton pump inhibitors (PPIs), can reduce acid production in the stomach.
4. Gastric surgery: Surgical procedures that remove part or all of the stomach can lead to achlorhydria.
5. Helicobacter pylori (H. pylori) infection: H. pylori bacteria can damage the stomach lining and reduce acid production.

Symptoms of achlorhydria may include:

1. Heartburn and regurgitation
2. Difficulty swallowing
3. Nausea and vomiting
4. Abdominal pain and bloating
5. Weight loss and malnutrition

If left untreated, achlorhydria can lead to complications such as:

1. Gastroesophageal reflux disease (GERD)
2. Peptic ulcers
3. Infections of the stomach and small intestine
4. Malnutrition and weight loss
5. Precancerous changes in the stomach lining

Treatment for achlorhydria usually involves addressing the underlying cause, such as eradicating H. pylori infection or replacing lost enzymes with supplements. In severe cases, medications that stimulate acid production or prostaglandin analogs may be prescribed to help protect the stomach lining. Proton pump inhibitors (PPIs) and histamine H2-receptor antagonists (H2RAs) are commonly used to reduce gastric acid production.

In summary, achlorhydria is a condition characterized by a lack of hydrochloric acid in the stomach, which can lead to various symptoms and complications. Treatment depends on identifying and addressing the underlying cause, and may involve medications to stimulate acid production or protect the stomach lining.

There are several types of thrombosis, including:

1. Deep vein thrombosis (DVT): A clot forms in the deep veins of the legs, which can cause swelling, pain, and skin discoloration.
2. Pulmonary embolism (PE): A clot breaks loose from another location in the body and travels to the lungs, where it can cause shortness of breath, chest pain, and coughing up blood.
3. Cerebral thrombosis: A clot forms in the brain, which can cause stroke or mini-stroke symptoms such as weakness, numbness, or difficulty speaking.
4. Coronary thrombosis: A clot forms in the coronary arteries, which supply blood to the heart muscle, leading to a heart attack.
5. Renal thrombosis: A clot forms in the kidneys, which can cause kidney damage or failure.

The symptoms of thrombosis can vary depending on the location and size of the clot. Some common symptoms include:

1. Swelling or redness in the affected limb
2. Pain or tenderness in the affected area
3. Warmth or discoloration of the skin
4. Shortness of breath or chest pain if the clot has traveled to the lungs
5. Weakness, numbness, or difficulty speaking if the clot has formed in the brain
6. Rapid heart rate or irregular heartbeat
7. Feeling of anxiety or panic

Treatment for thrombosis usually involves medications to dissolve the clot and prevent new ones from forming. In some cases, surgery may be necessary to remove the clot or repair the damaged blood vessel. Prevention measures include maintaining a healthy weight, exercising regularly, avoiding long periods of immobility, and managing chronic conditions such as high blood pressure and diabetes.

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.

Glioblastomas are highly malignant tumors that can grow rapidly and infiltrate surrounding brain tissue, making them difficult to remove surgically. They often recur after treatment and are usually fatal within a few years of diagnosis.

The symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory or cognitive function.

Glioblastomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and a biopsy to confirm the presence of cancerous cells. Treatment typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy to slow the growth of any remaining cancerous cells.

Prognosis for glioblastoma is generally poor, with a five-year survival rate of around 5% for newly diagnosed patients. However, the prognosis can vary depending on factors such as the location and size of the tumor, the patient's age and overall health, and the effectiveness of treatment.

2. Our research focuses on identifying the genetic mutations that contribute to experimental melanoma and developing targeted therapies.
3. The patient's experimental melanoma had spread to her lungs and liver, so we recommended chemotherapy and immunotherapy treatments.

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

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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

The tumor cells are typically small, uniform, and well-differentiated, with a distinct cell border and a central nucleus. The tumor cells are often arranged in a glandular or tubular pattern, which is characteristic of this type of cancer.

Carcinoma, Lewis lung usually affects older adults, with the median age at diagnosis being around 60 years. Men are slightly more likely to be affected than women. The main risk factor for developing this type of cancer is smoking, although it can also occur in people who have never smoked.

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

* Chest pain or discomfort
* Coughing up blood
* Shortness of breath
* Fatigue
* Weight loss

If you suspect you may have Carcinoma, Lewis lung or are experiencing any of these symptoms, it is important to consult a healthcare professional for an accurate diagnosis and appropriate treatment.

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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 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.

A group of autoimmune blistering diseases that are characterized by the formation of large, tense bullae on the skin and mucous membranes. These diseases are caused by abnormal immunological responses to certain antigens, which lead to the production of autoantibodies that attack the basement membrane zone of the skin and mucous membranes, causing damage and blister formation.

There are several types of pemphigoid, bullous diseases, including:

* Pemphigoid, benign chronic
* Pemphigoid, severe
* Bullous pemphigoid
* Epidermolysis bullosa acquisita

Symptoms of pemphigoid, bullous diseases may include:

* Blisters on the skin and mucous membranes
* Redness and swelling around the blisters
* Itching or pain
* Fever

Diagnosis of pemphigoid, bullous diseases is based on a combination of clinical findings, laboratory tests, and biopsy. Treatment involves the use of corticosteroids, immunosuppressive drugs, and antibiotics to manage symptoms and prevent complications.

There are several types of gliomas, including:

1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.

The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.

Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.

The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.

* Peripheral T-cell lymphoma (PTCL): This is a rare type of T-cell lymphoma that can develop in the skin, lymph nodes, or other organs.
* Cutaneous T-cell lymphoma (CTCL): This is a type of PTCL that affects the skin and can cause lesions, rashes, and other skin changes.
* Anaplastic large cell lymphoma (ALCL): This is a rare subtype of PTCL that can develop in the lymph nodes, spleen, or bone marrow.
* Adult T-cell leukemia/lymphoma (ATLL): This is a rare and aggressive subtype of PTCL that is caused by the human T-lymphotropic virus type 1 (HTLV-1).

Symptoms of T-cell lymphoma can include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Skin lesions or rashes

Treatment options for T-cell lymphoma depend on the subtype and stage of the cancer, but may include:

* Chemotherapy
* Radiation therapy
* Immunotherapy
* Targeted therapy

Prognosis for T-cell lymphoma varies depending on the subtype and stage of the cancer, but in general, the prognosis for PTCL is poorer than for other types of non-Hodgkin lymphoma. However, with prompt and appropriate treatment, many people with T-cell lymphoma can achieve long-term remission or even be cured.

Benign ovarian neoplasms include:

1. Serous cystadenoma: A fluid-filled sac that develops on the surface of the ovary.
2. Mucinous cystadenoma: A tumor that is filled with mucin, a type of protein.
3. Endometrioid tumors: Tumors that are similar to endometrial tissue (the lining of the uterus).
4. Theca cell tumors: Tumors that develop in the supportive tissue of the ovary called theca cells.

Malignant ovarian neoplasms include:

1. Epithelial ovarian cancer (EOC): The most common type of ovarian cancer, which arises from the surface epithelium of the ovary.
2. Germ cell tumors: Tumors that develop from germ cells, which are the cells that give rise to eggs.
3. Stromal sarcomas: Tumors that develop in the supportive tissue of the ovary.

Ovarian neoplasms can cause symptoms such as pelvic pain, abnormal bleeding, and abdominal swelling. They can also be detected through pelvic examination, imaging tests such as ultrasound and CT scan, and biopsy. Treatment options for ovarian neoplasms depend on the type, stage, and location of the tumor, and may include surgery, chemotherapy, and radiation therapy.

There are several types of muscular dystrophies, including:

1. Duchenne muscular dystrophy (DMD): This is the most common form of muscular dystrophy, affecting males primarily. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, wheelchair dependence, and shortened lifespan.
2. Becker muscular dystrophy (BMD): This is a less severe form of muscular dystrophy than DMD, affecting both males and females. It is caused by a mutation in the dystrophin gene and is characterized by progressive muscle weakness, but with a milder course than DMD.
3. Limb-girdle muscular dystrophy (LGMD): This is a group of disorders that affect the muscles around the shoulders and hips, leading to progressive weakness and degeneration. There are several subtypes of LGMD, each with different symptoms and courses.
4. Facioscapulohumeral muscular dystrophy (FSHD): This is a rare form of muscular dystrophy that affects the muscles of the face, shoulder, and upper arm. It is caused by a mutation in the D4Z4 repeat on chromosome 4.
5. Myotonic dystrophy: This is the most common adult-onset form of muscular dystrophy, affecting both males and females. It is characterized by progressive muscle stiffness, weakness, and wasting, as well as other symptoms such as cataracts, myotonia, and cognitive impairment.

There is currently no cure for muscular dystrophies, but various treatments are available to manage the symptoms and slow the progression of the disease. These include physical therapy, orthotics and assistive devices, medications to manage pain and other symptoms, and in some cases, surgery. Researchers are actively working to develop new treatments and a cure for muscular dystrophies, including gene therapy, stem cell therapy, and small molecule therapies.

It's important to note that muscular dystrophy can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner, depending on the specific type of dystrophy. This means that the risk of inheriting the condition depends on the mode of inheritance and the presence of mutations in specific genes.

In summary, muscular dystrophy is a group of genetic disorders characterized by progressive muscle weakness and degeneration. There are several types of muscular dystrophy, each with different symptoms and courses. While there is currently no cure for muscular dystrophy, various treatments are available to manage the symptoms and slow the progression of the disease. Researchers are actively working to develop new treatments and a cure for muscular dystrophy.

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.

These proteins are essential for white blood cells to stick together and migrate through the blood vessels into tissues, where they can fight off infections. The symptoms of Leukocyte Adhesion Deficiency syndrome vary depending on which gene is mutated and the severity of the mutation.

Some of the common symptoms include recurrent or persistent infections, poor wound healing, delayed development of the skin and mucous membranes, and difficulty fighting off certain types of bacteria, viruses, and fungi. The diagnosis of Leukocyte Adhesion Deficiency syndrome is based on a combination of clinical findings, laboratory tests that measure the function of white blood cells, and genetic analysis that identifies mutations in one of the genes involved in leukocyte adhesion.

Treatment for Leukocyte Adhesion Deficiency syndrome usually involves antibiotics to prevent or treat infections, topical creams or ointments to promote wound healing, and occasionally immunoglobulin replacement therapy to boost the immune system.

Several types of Leukocyte Adhesion Deficiency syndrome exist, each caused by a mutation in a different gene involved in leukocyte adhesion. The most common form of this disorder is called LAMA2 deficiency or Hereditary Angioedema with Giant Lymph Node.

Overall, early diagnosis and appropriate treatment can help manage symptoms and prevent complications associated with Leukocyte Adhesion Deficiency syndrome.

Leukocyte adhesion deficiency (LAD) is a group of rare genetic disorders characterized by impaired leukocyte trafficking and immune dysfunction. The disorders are caused by mutations in genes encoding proteins involved in leukocyte adhesion and migration, such as integrins and chemokine receptors.

There are several types of LAD, each with distinct clinical features and symptoms. The most common form of the disorder is LAMA2 deficiency, which affects approximately 1 in 50,000 individuals worldwide. Other forms of LAD include CD1a and CD1b deficiencies, which are less common but can have overlapping clinical features with LAMA2 deficiency.

The primary symptom of LAD is recurrent skin infections, particularly in childhood. Patients may also experience respiratory infections, gastrointestinal infections, and abscesses. In addition, some patients with LAD may develop chronic inflammation and fibrosis, which can lead to severe complications such as renal failure or blindness.

The diagnosis of LAD is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include flow cytometry, which can assess leukocyte function and adhesion properties, and molecular genetic testing, which can identify mutations in genes encoding integrins or other adhesion molecules.

Treatment of LAD typically involves antibiotics for recurrent skin and soft tissue infections, as well as management of any underlying chronic inflammation or fibrosis. In some cases, bone marrow transplantation may be considered as a curative therapy.

Overall, LAD is a rare and complex disorder that requires careful diagnosis and management by a multidisciplinary team of healthcare professionals. With appropriate treatment, many patients with LAD can lead active and productive lives, although some may experience ongoing complications or lifelong immune dysfunction.

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.

Types of experimental neoplasms include:

* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.

The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.

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.

SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.

SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.

Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.

The exact cause of leiomyosarcoma is not known, but it is believed to be linked to genetic mutations that occur in the smooth muscle cells. It can occur at any age, but it is more common in women, especially after menopause.

Symptoms of leiomyosarcoma may include:

* Abnormal bleeding or discharge from the uterus or cervix
* Pelvic pain or discomfort
* A mass or lump in the abdomen or pelvis
* Weakness, fatigue, or fever

If leiomyosarcoma is suspected, a healthcare provider may perform a variety of tests to confirm the diagnosis, including:

* Pelvic examination and imaging tests, such as ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI) to visualize the tumor.
* Biopsy, where a sample of tissue is removed from the suspected tumor and examined under a microscope for cancer cells.

Treatment options for leiomyosarcoma depend on the location, size, and stage of the cancer, as well as the patient's age and overall health. Surgery is often the primary treatment, and may involve removing the uterus, cervix, or other affected organs. Radiation therapy and chemotherapy may also be used to kill any remaining cancer cells.

Overall, leiomyosarcoma is a rare and aggressive form of cancer that requires prompt medical attention if symptoms persist or worsen over time. With proper treatment, many people with leiomyosarcoma can achieve long-term survival and a good quality of life.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

Some common types of bone neoplasms include:

* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.

Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.

There are several subtypes of liposarcoma, including:

1. Well-differentiated liposarcoma (WDLS): This is the most common type of liposarcoma and tends to grow slowly.
2. Dedifferentiated liposarcoma (DDLS): This type of liposarcoma grows more quickly than WDLS and can be more aggressive.
3. Myxoid liposarcoma: This is a rare subtype that tends to grow slowly and has a good prognosis.
4. Pleomorphic liposarcoma: This is the most aggressive type of liposarcoma and can be difficult to treat.

The exact cause of liposarcoma is not known, but it is believed to be linked to genetic mutations that occur in the fat cells. Risk factors for developing liposarcoma include a family history of the condition, previous radiation exposure, and certain inherited conditions such as neurofibromatosis type 1 (NF1) or Li-Fraumeni syndrome.

Symptoms of liposarcoma may include a soft tissue mass, pain, swelling, and limited mobility in the affected area. Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and PET scans, as well as a biopsy to confirm the presence of cancer cells.

Treatment for liposarcoma depends on the size, location, and stage of the cancer, as well as the patient's overall health. Surgery is the primary treatment, and may involve removing the tumor and some surrounding tissue. In some cases, radiation therapy or chemotherapy may also be used to shrink the tumor before surgery or to kill any remaining cancer cells after surgery. The prognosis for liposarcoma varies depending on the subtype and stage of the cancer, but in general, the earlier the diagnosis and treatment, the better the outlook.

Peritoneal neoplasms are relatively rare, but they can be aggressive and difficult to treat. The most common types of peritoneal neoplasms include:

1. Peritoneal mesothelioma: This is the most common type of peritoneal neoplasm and arises from the mesothelial cells that line the abdominal cavity. It is often associated with asbestos exposure.
2. Ovarian cancer: This type of cancer originates in the ovaries and can spread to the peritoneum.
3. Appendiceal cancer: This type of cancer arises in the appendix and can spread to the peritoneum.
4. Pseudomyxoma peritonei: This is a rare type of cancer that originates in the abdominal cavity and resembles a mucin-secreting tumor.
5. Primary peritoneal cancer: This type of cancer originates in the peritoneum itself and can be of various types, including adenocarcinoma, squamous cell carcinoma, and sarcoma.

The symptoms of peritoneal neoplasms vary depending on the location and size of the tumor, but may include abdominal pain, distension, and difficulty eating or passing stool. Treatment options for peritoneal neoplasms depend on the type and stage of the cancer, but may include surgery, chemotherapy, and radiation therapy. Prognosis for peritoneal neoplasms is generally poor, with a five-year survival rate of around 20-30%.

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 several possible causes of thrombocytopenia, including:

1. Immune-mediated disorders such as idiopathic thrombocytopenic purpura (ITP) or systemic lupus erythematosus (SLE).
2. Bone marrow disorders such as aplastic anemia or leukemia.
3. Viral infections such as HIV or hepatitis C.
4. Medications such as chemotherapy or non-steroidal anti-inflammatory drugs (NSAIDs).
5. Vitamin deficiencies, especially vitamin B12 and folate.
6. Genetic disorders such as Bernard-Soulier syndrome.
7. Sepsis or other severe infections.
8. Disseminated intravascular coagulation (DIC), a condition where blood clots form throughout the body.
9. Postpartum thrombocytopenia, which can occur in some women after childbirth.

Symptoms of thrombocytopenia may include easy bruising, petechiae (small red or purple spots on the skin), and prolonged bleeding from injuries or surgical sites. Treatment options depend on the underlying cause but may include platelet transfusions, steroids, immunosuppressive drugs, and in severe cases, surgery.

In summary, thrombocytopenia is a condition characterized by low platelet counts that can increase the risk of bleeding and bruising. It can be caused by various factors, and treatment options vary depending on the underlying cause.

Junctional EB (JEB) is a type of EB that affects the space between cells in the skin, known as the basement membrane zone. This condition is caused by mutations in the genes that encode proteins involved in the structure and function of the basement membrane.

Symptoms of JEB typically appear at birth or in early childhood and may include:

* Skin blisters and sores, often on the hands, feet, and other areas exposed to friction
* Thickening and scarring of the skin
* Delayed healing of wounds
* Skin cancer risk

JEB is diagnosed through a combination of clinical evaluation, genetic testing, and histopathological analysis of skin biopsies. There is no cure for JEB, but various treatments can help manage symptoms and prevent complications. These may include:

* Wound care and dressing
* Pain management with medication
* Physical therapy to maintain joint mobility and prevent contractures
* Surgery to remove scar tissue or repair damaged skin

The prognosis for JEB varies depending on the severity of the condition. Some individuals with mild forms of JEB may lead relatively normal lives, while those with more severe forms of the condition may experience significant disability and reduced life expectancy.

Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.

There are many different types of fibrosis, including:

* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.

Fibrosis can be diagnosed through a variety of methods, including:

* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.

There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:

* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.

It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.

There are several types of stomach neoplasms, including:

1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.

The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.

Examples of 'Adenocarcinoma, Mucinous' in medical literature:

* The patient was diagnosed with adenocarcinoma, mucinous type, in their colon after undergoing a colonoscopy and biopsy. (From the Journal of Clinical Oncology)

* The patient had a history of adenocarcinoma, mucinous type, in their breast and was being monitored for potential recurrence. (From the Journal of Surgical Oncology)

* The tumor was found to be an adenocarcinoma, mucinous type, with a high grade and was treated with surgery and chemotherapy. (From the Journal of Gastrointestinal Oncology)

Synonyms for 'Adenocarcinoma, Mucinous' include:

* Mucinous adenocarcinoma
* Colon adenocarcinoma, mucinous type
* Rectal adenocarcinoma, mucinous type
* Adenocarcinoma of the colon and rectum, mucinous type.

There are several factors that can contribute to bone resorption, including:

1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.

Bone resorption can be diagnosed through a range of tests, including:

1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.

Treatment for bone resorption depends on the underlying cause and may include:

1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.

Blisters are caused by friction or rubbing against a surface, which causes the top layer of skin to separate from the underlying layer. This separation creates a space that fills with fluid, forming a blister. Blisters can also be caused by burns, chemical exposure, or other types of injury.

There are different types of blisters, including:

1. Friction blisters: These are the most common type of blister and are caused by friction or rubbing against a surface. They are often seen on the hands, feet, and buttocks.
2. Burn blisters: These are caused by burns and can be more severe than friction blisters.
3. Chemical blisters: These are caused by exposure to chemicals and can be very painful.
4. Blisters caused by medical conditions: Certain medical conditions, such as epidermolysis bullosa (a genetic disorder that affects the skin), can cause blisters to form easily.

Blisters can be treated in several ways, depending on their size and location. Small blisters may not require treatment and can heal on their own within a few days. Larger blisters may need to be drained and covered with a bandage to prevent infection. In severe cases, surgical intervention may be necessary.

Preventing blisters is key to avoiding the discomfort and pain they can cause. To prevent blisters, it is important to:

1. Wear properly fitting shoes and clothing to reduce friction.
2. Use lubricating creams or powders to reduce friction.
3. Take regular breaks to rest and allow the skin to recover.
4. Avoid using harsh chemicals or detergents that can cause irritation.
5. Keep the affected area clean and dry to prevent infection.

In conclusion, blisters are a common and uncomfortable condition that can be caused by a variety of factors. While they can be treated and managed, prevention is key to avoiding the discomfort and pain they can cause. By taking steps to prevent blisters and seeking medical attention if they do occur, individuals can reduce their risk of developing this uncomfortable condition.

There are two main forms of alpha-Thalassemia:

1. Alpha-thalassemia major (also known as Hemoglobin Bart's hydrops fetalis): This is a severe form of the disorder that can cause severe anemia, enlarged spleen, and death in infancy. It is caused by a complete absence of one or both of the HBA1 or HBA2 genes.
2. Alpha-thalassemia minor (also known as Hemoglobin carrier state): This form of the disorder is milder and may not cause any symptoms at all. It is caused by a partial deletion of one or both of the HBA1 or HBA2 genes.

People with alpha-thalassemia minor may have slightly lower levels of hemoglobin and may be more susceptible to anemia, but they do not typically experience any severe symptoms. Those with alpha-thalassemia major, on the other hand, are at risk for serious complications such as anemia, infections, and organ failure.

There is no cure for alpha-thalassemia, but treatment options include blood transfusions, iron chelation therapy, and management of associated complications. Screening for alpha-thalassemia is recommended for individuals who are carriers of the disorder, as well as for those who have a family history of the condition.

Evander M, Frazer IH, Payne E, Qi YM, Hengst K, McMillan NA (March 1997). "Identification of the alpha6 integrin as a candidate ... McMillan NA, Payne E, Frazer IH, Evander M (September 1999). "Expression of the alpha6 integrin confers papillomavirus binding ... likely via the alpha-6 beta-4 integrin, and transported to membrane-enclosed vesicles called endosomes. The capsid protein L2 ...
Integrin alpha-6 is a protein that in humans is encoded by the ITGA6 gene. The ITGA6 protein product is the integrin alpha ... For example, alpha 6 may combine with beta 4 in the integrin referred to as TSP180, or with beta 1 in the integrin VLA-6. ... "Entrez Gene: ITGA6 integrin, alpha 6". De Arcangelis A, Hamade H, Alpy F, Normand S, Bruyère E, Lefebvre O, et al. (October ... Tani TT, Mercurio AM (September 2001). "PDZ interaction sites in integrin alpha subunits. T14853, TIP/GIPC binds to a type I ...
Bretscher, MS (1992). "Circulating integrins: alpha5-beta1, alpha6-beta4 and Mac-1, but not alpha3-beta1, alpha4-beta1 or LFA-1 ... For a cell to move, it is necessary to bring a fresh supply of "feet" (proteins called integrins, which attach a cell to the ...
"The PDZ domain of TIP-2/GIPC interacts with the C-terminus of the integrin alpha5 and alpha6 subunits". Matrix Biol. 21 (2): ... Tani TT, Mercurio AM (September 2001). "PDZ interaction sites in integrin alpha subunits. T14853, TIP/GIPC binds to a type I ... Tani TT, Mercurio AM (2001). "PDZ interaction sites in integrin alpha subunits. T14853, TIP/GIPC binds to a type I recognition ...
Antibodies to the beta-4 integrin subunit of alpha-6-beta-4 integrin is shown to be associated with ocular disease while oral ... Alpha-6-beta-4 integrin Type VII collagen. In contrast to the target of the N-terminus of BP180 that is located in the ... Antigens include 180-kD bullous pemphigoid antigen (BP180), laminin 332, beta-4-integrin, and other antigens that are not fully ... the major human keratinocyte integrin ligand, is a target in both an acquired autoimmune and an inherited subepidermal ...
... receptor Pathway Transforming growth factor beta receptor pathway Tumor necrosis factor alpha pathway Alpha6 Beta4 Integrin ...
ALDH alkaline phosphatase alpha6-integrin Anti-WNT2B monoclonal antibody antithrombin III (AT) asialo GM1 Bcl-2 Beta- ... Hall PE, Lathia JD, Miller NG, Caldwell MA, ffrench-Constant C (September 2006). "Integrins are markers of human neural stem ... Shinohara T, Avarbock MR, Brinster RL (May 1999). "β1- and α6-integrin are surface markers on mouse spermatogonial stem cells ... galactosidase (β-gal) of ROSA26 mice beta1-integrin bromodeoxyuridine c-kit (CD117) c-Met C1qR(p) END (CD105) PROM1 (CD133) ...
... integrin alpha4 MeSH D23.050.301.264.035.293 - integrin alpha5 MeSH D23.050.301.264.035.296 - integrin alpha6 MeSH D23.050. ... integrin alpha4 MeSH D23.101.100.110.294 - integrin alpha5 MeSH D23.101.100.110.297 - integrin alpha6 MeSH D23.101.100.110.298 ... integrin alphav MeSH D23.101.100.110.299 - integrin beta3 MeSH D23.101.100.110.302 - integrin beta4 MeSH D23.101.100.110.400 - ... integrin alpha1 MeSH D23.050.301.264.035.287 - integrin alpha2 MeSH D23.050.301.264.035.289 - integrin alpha3 MeSH D23.050. ...
... integrin alpha4 MeSH D12.776.543.750.705.408.100.500 - integrin alpha5 MeSH D12.776.543.750.705.408.100.550 - integrin alpha6 ... integrin alpha1 MeSH D12.776.543.750.705.408.100.350 - integrin alpha2 MeSH D12.776.543.750.705.408.100.400 - integrin alpha3 ... integrin alpha2beta1 MeSH D12.776.543.550.625.379 - integrin alpha5beta1 MeSH D12.776.543.550.625.419 - integrin alpha6beta1 ... integrin alpha1beta1 MeSH D12.776.543.750.072.200 - integrin alpha2beta1 MeSH D12.776.543.750.072.300 - integrin alpha3beta1 ...
1999). "Characterization of UDP-N-acetylglucosamine:alpha-6-d-mannoside beta-1,6-N-acetylglucosaminyltransferase V from a human ... 2007). "Increase in beta1-6 GlcNAc branching caused by N-acetylglucosaminyltransferase V directs integrin beta1 stability in ...
The 2014 Ju-Jitsu World Championship were the 12th edition of the Ju-Jitsu World Championships, and were held in Paris, France from November 28 to November 30, 2014. 28.11.2014 - Men's and Women's Fighting System, Men's and Women's Jiu-Jitsu (ne-waza), Men's Duo System - Classic 29.11.2014 - Men's and Women's Fighting System, Men's and Women's Jiu-Jitsu (ne-waza), Women's Duo System - Classic 30.11.2014 - Men's Jiu-Jitsu (ne-waza), Mixed Duo System - Classic, Team event Vincent MATCZAK (2014-09-30). "4TH INVITAION TO WORLD CHAMPIONSHIP 2014" (PDF). Retrieved 2019-11-28.[dead link] Online results Official results (PDF) Mixed team event results (PDF) (All articles with dead external links, Articles with dead external links from April 2022, Ju-Jitsu World Championships, 2014 in French sport ...
Bolley L. "Bo" Johnson (born November 15, 1951) is an American politician from the state of Florida. A member of the Democratic Party, Johnson was a member of the Florida House of Representatives, and served as the Speaker of the Florida House of Representatives. Johnson is from Milton, Florida. His father and grandfather served as county commissioners for Santa Rosa County, Florida. Johnson graduated from Milton High School, and became the first member of his family to attend college. He received his bachelor's degree from Florida State University. Johnson volunteered for Mallory Horne when Horne served as the president of the Florida Senate. At the age of 22, Johnson met Lawton Chiles, then a member of the United States Senate, who hired him as a legislative aide in 1973. Johnson was elected to the Florida House of Representatives, representing the 4th district from November 7, 1978 to November 3, 1992. He also served the 1st district from November 3, 1992 to November 8, 1994. He became the ...
... may refer to: Don't Say No (Billy Squier album), a 1981 album by American rock singer Billy Squier, and its title track Don't Say No (Seohyun EP), a 2016 extended play by South Korean pop singer Seohyun, and its title track "Don't Say No" (Tom Tom Club song), from the 1988 album Boom Boom Chi Boom Boom "Don't Say No", by Robbie Williams from the 2005 album Intensive Care "Don't Say No Tonight", a 1985 single by Eugene Wilde This disambiguation page lists articles associated with the title Don't Say No. If an internal link led you here, you may wish to change the link to point directly to the intended article. (Disambiguation pages with short descriptions, Short description is different from Wikidata, All article disambiguation pages, All disambiguation pages, Disambiguation pages ...
The Dewoitine 37 was the first of a family of 1930s French-built monoplane fighter aircraft. The D.37 was a single-seat aircraft of conventional configuration. Its fixed landing gear used a tailskid. The open cockpit was located slightly aft of the parasol wing. The radial engine allowed for a comparatively wide fuselage and cockpit. Design of this machine was by SAF-Avions Dewoitine but owing to over work at that companies plant at the time, manufacture of the D.37/01 was transferred to Lioré et Olivier. They were high-wing monoplanes of all-metal construction with valve head blisters on their engine cowlings. The first prototype flew in October 1931. Flight testing resulted in the need for multiple revisions in both engine and airframe, so it was February 1934 before the second prototype flew. Its performance prompted the French government to order for 28 for the Armée de l'Air and Aéronavale. The Lithuanian government ordered 14 that remained in service with their Air Force until 1936, ...
The Noor-ul-Ain (Persian: نور العين, lit. 'the light of the eye') is one of the largest pink diamonds in the world, and the centre piece of the tiara of the same name. The diamond is believed to have been recovered from the mines of Golconda, Hyderabad in India. It was first in possession with the nizam Abul Hasan Qutb Shah, later it was given as a peace offering to the Mughal emperor Aurangazeb when he defeated him in a siege. It was brought into the Iranian Imperial collection after the Persian king Nader Shah Afshar looted Delhi in the 18th century.[citation needed] The Noor-ul-Ain is believed to have once formed part of an even larger gem called the Great Table diamond. That larger diamond is thought to have been cut in two, with one section becoming the Noor-ul-Ain and the other the Daria-i-Noor diamond. Both of these pieces are currently part of the Iranian Crown Jewels. The Noor-ul-Ain is the principal diamond mounted in a tiara of the same name made for Iranian Empress Farah ...
The Benoist Land Tractor Type XII was one of the first enclosed cockpit, tractor configuration aircraft built. Benoist used "Model XII" to several aircraft that shared the same basic engine and wing design, but differed in fuselage and control surfaces. The Type XII was a tractor-engined conversion of the model XII headless pusher aircraft that resembled the Curtiss pusher aircraft. Demonstration pilots used Benoist aircraft to demonstrate the first parachute jumps, and the tractor configuration was considered much more suitable for the task. The first example named the "Military Plane" had a small box frame covered fuselage that left the occupants mostly exposed to the wind. The later model XII "Cross Country Plane" had a full fuselage that occupants sat inside of. The first tractor biplane used a wooden fuselage with a small seat on top. The wings were covered with a Goodyear rubberized cloth. The first model XII was built in the spring of 1912. On 1 March 1912, Albert Berry used a headless ...
... (also known as Yalmotx in Qʼanjobʼal) is a town, with a population of 17,166 (2018 census), and a municipality in the Guatemalan department of Huehuetenango. It is situated at 1450 metres above sea level. It covers a terrain of 1,174 km². The annual festival is April 29-May 4. Barillas has a tropical rainforest climate (Af) with heavy to very heavy rainfall year-round and extremely heavy rainfall from June to August. Citypopulation.de Population of departments and municipalities in Guatemala Citypopulation.de Population of cities & towns in Guatemala "Climate: Barillas". Climate-Data.org. Retrieved July 26, 2020. Muni in Spanish Website of Santa Cruz Barillas Coordinates: 15°48′05″N 91°18′45″W / 15.8014°N 91.3125°W / 15.8014; -91.3125 v t e (Articles with short description, Short description is different from Wikidata, Pages using infobox settlement with no coordinates, Articles containing Q'anjob'al-language text, Coordinates on Wikidata, ...
Maria Margaret La Primaudaye Pollen (10 April 1838 - c. 1919), known as Minnie, was a decorative arts collector. As Mrs John Hungerford Pollen, she became known during the early-twentieth century as an authority on the history of textiles, publishing Seven Centuries of Lace in 1908. Maria Margaret La Primaudaye was born into a Huguenot family on 10 April 1838, the third child of the Revd Charles John La Primaudaye, a descendant of Pierre de La Primaudaye. She was educated in Italy. Her family converted to Catholicism in 1851, and it was in Rome that her father met another recent English convert, John Hungerford Pollen, previously an Anglican priest and a decorative artist. She became engaged to Pollen, who was then seventeen years her senior, in the summer of 1854, and was married in the church of Woodchester monastery, near Stroud, Gloucester, on 18 September 1855. The Pollens initially settled in Dublin, where John Hungerford Pollen had been offered the professorship of fine arts at the ...
Ronald Robert Fogleman (born January 27, 1942) is a retired United States Air Force general who served as the 15th Chief of Staff of the Air Force from 1994 to 1997 and as Commanding General of the United States Transportation Command from 1992 to 1994. A 1963 graduate from the United States Air Force Academy, he holds a master's degree in military history and political science from Duke University. A command pilot and a parachutist, he amassed more than 6,800 flying hours in fighter, transport, tanker and rotary wing aircraft. He flew 315 combat missions and logged 806 hours of combat flying in fighter aircraft. Eighty of his missions during the Vietnam War were as a "Misty FAC" in the F-100F Super Sabre at Phù Cát Air Base, South Vietnam between 25 December 1968 and 23 April 1969. Fogleman was shot down in Vietnam in 1968, while piloting an F-100. He was rescued by clinging to an AH-1 Cobra attack helicopter that landed at the crash site. In early assignments he instructed student pilots, ...
Peachtree Street" is a 1950 song co-written and recorded by Frank Sinatra in a duet with Rosemary Clooney. The song was released as a Columbia Records single. Frank Sinatra co-wrote the song with Leni Mason and Jimmy Saunders. Mason composed the music while Sinatra and Saunders wrote the lyrics. The song was arranged by George Siravo The song was released as an A side Columbia 10" 78 single, Catalog Number 38853, Matrix Number CO-43100-1 and as a 7" 33, 1-669. The B side was the re-issued "This Is the Night." Neither of the songs charted. The subject of the song is a stroll down the street in Atlanta, Georgia of the same name. Sinatra originally intended Dinah Shore to sing the duet with him. When Shore declined, Clooney was asked. The song was recorded on April 8, 1950. The song features spoken asides by Sinatra and Clooney. Rosemary Clooney asks: "Say, Frank, you wanna take a walk?" Frank Sinatra replies: "Sure, sweetie, just pick a street." He noted how there were no peach trees on the ...
... is a painting by American illustrator Norman Rockwell that depicts a Boy Scout in full uniform standing in front of a waving American flag. It was originally created by Rockwell in 1942 for the 1944 Brown & Bigelow Boy Scout Calendar. The model, Bob Hamilton, won a contest to be in the painting and personally delivered a print to the Vice President of the United States at the time, Henry A. Wallace. The painting was created to encourage Scouts to participate in the war effort during World War II. The name of the painting, We, Too, Have a Job to Do, comes from a slogan that the Boy Scouts of America used in 1942 to rally scouts to support the troops by collecting metal and planting victory gardens. The model, Bob Hamilton, won a contest with his local council in Albany, New York, to be depicted in the painting. He traveled to Rockwell's studio in Arlington, Vermont, to model for Rockwell. Since Hamilton was a scout, the uniform shown in the painting was his, unlike some ...
At least 33[failed verification] people were killed by a fuel tanker explosion in Tleil, Akkar District, Lebanon on 15 August 2021. The disaster was reportedly exacerbated by the ongoing Lebanese liquidity crisis; in which the Lebanese pound has plummeted and fuel has been in short supply. The survivors were evacuated by the Lebanese Red Cross. An investigation is underway. The fuel tanker had been confiscated by the Lebanese Armed Forces from black marketeers, the fuel was then distributed/taken by the locals. The son of the man whose land the fuel tanker was located on, was later arrested, accused of deliberately causing the explosion. Agencies (2021-08-15). "At least 20 killed and 79 injured in fuel tank explosion in Lebanon". the Guardian. Retrieved 2021-08-15. "Lebanon fuel explosion kills 22 and injures dozens more". The Independent. 2021-08-15. Archived from the original on 2021-08-15. Retrieved 2021-08-15. "Lebanon: At least 20 dead and dozens injured after fuel tank explodes as ...
The Straubing Tigers are a professional men's ice hockey team, based in Straubing, Germany, that competes in the Deutsche Eishockey Liga. Straubing plays its home games at the Eisstadion am Pulverturm, which has a capacity of 5,800 spectators. Promoted to the DEL in 2006, and operating with one of the league's smallest budgets, the team could finish no better than twelfth before the 2011-12 DEL season, when it reached the semi-finals of the playoffs. Their greatest success so far is the qualification for the season 2020-21 of the Champions Hockey League. In 1941, the then 14-year-old Max Pielmaier and his friends Max Pellkofer and Harry Poiger founded the first hockey team in Straubing. The first official game took place on the first of February 1942 in Hof and was lost by a score of 0:1. In the following year there were several games against other Bavarian teams. The game against Landshut on 31 January. 1943 was the last game during the second World War, because the young players also had to ...
Leina is a village in Saaremaa Parish, Saare County in western Estonia. Before the administrative reform in 2017, the village was in Pihtla Parish. "Lisa. Asustusüksuste nimistu" (PDF). haldusreform.fin.ee (in Estonian). Rahandusministeerium. Retrieved 5 December 2017. "Saaremaa külad endiste valdade piires". www.saaremaa.ee (in Estonian). Archived from the original on 3 December 2017. Retrieved 5 December 2017. Coordinates: 58°17′10″N 22°46′26″E / 58.28611°N 22.77389°E / 58.28611; 22.77389 v t e (CS1 Estonian-language sources (et), Articles with short description, Short description is different from Wikidata, Pages using infobox settlement with no map, Pages using infobox settlement with no coordinates, Saaremaa Parish, Coordinates on Wikidata, Villages in Saare County, All stub articles, Saare County geography stubs ...
A sestiere (plural: sestieri) is a subdivision of certain Italian towns and cities. The word is from sesto ('sixth'), so it is thus used only for towns divided into six districts. The best-known example is the sestieri of Venice, but Ascoli Piceno, Genoa, Milan and Rapallo, for example, were also divided into sestieri. The medieval Lordship of Negroponte, on the island of Euboea, was also at times divided into six districts, each with a separate ruler, through the arbitration of Venice, which were known as sestieri. The island of Crete, a Venetian colony (the "Kingdom of Candia") from the Fourth Crusade, was also divided into six parts, named after the sestieri of Venice herself, while the capital Candia retained the status of a comune of Venice. The island of Burano north of Venice is also subdivided into sestieri. A variation of the word is occasionally found: the comune of Leonessa, for example, is divided into sesti or sixths. Other Italian towns with fewer than six official districts are ...
The Island Image is a Chesapeake Bay log canoe, built in 1885 at Elliot's Island, Maryland, by Herman Jones and Isaac Moore. She is 29'-8½" long with a beam of 5-10¼", and has a straight, raking stem and a sharp stern. It is privately owned, and races under No. 17. She one of the last 22 surviving traditional Chesapeake Bay racing log canoes that carry on a tradition of racing on the Eastern Shore of Maryland that has existed since the 1840s. She is located at Chestertown, Kent County, Maryland. She was listed on the National Register of Historic Places in 1985. "National Register Information System". National Register of Historic Places. National Park Service. April 15, 2008. "Maryland Historical Trust". ISLAND IMAGE (log canoe). Maryland Historical Trust. 2008-06-14. "Island Image #17 , CBLCSA". Island Image. Chesapeake Bay Log Sailing Canoe Association. 2010-07-24. Archived from the original on 2011-07-08. Retrieved 2010-07-29. ISLAND IMAGE (log canoe), Kent County, including photo in 1984, ...
... (Persian: دهستان بردخون) is a rural district (dehestan) in the Bord Khun District of Deyr County, Bushehr Province, Iran. At the 2006 census, its population was 1,115, in 234 families. The rural district has 14 villages. "Census of the Islamic Republic of Iran, 1385 (2006)" (Excel). Statistical Center of Iran. Archived from the original on 2011-11-11. Coordinates: 27°58′N 51°32′E / 27.967°N 51.533°E / 27.967; 51.533 v t e (Articles with short description, Short description matches Wikidata, Pages using infobox settlement with no map, Pages using infobox settlement with no coordinates, Articles containing Persian-language text, Coordinates on Wikidata, Rural Districts of Bushehr Province, Deyr County, All stub articles, Deyr County geography stubs ...
... is a disease of camels caused by the camelpox virus (CMPV) of the family Poxviridae, subfamily Chordopoxvirinae, and the genus Orthopoxvirus. It causes skin lesions and a generalized infection. Approximately 25% of young camels that become infected will die from the disease, while infection in older camels is generally more mild. Although rare, the infection may spread to the hands of those that work closely with camels. The camelpox virus that causes camelpox is an orthopoxvirus that is very closely related to the variola virus that causes smallpox. It is a large, brick-shaped, enveloped virus that ranges in size from 265-295 nm. The viral genetic material is contained in a linear double-stranded DNA consisting of 202,182 tightly packed base pairs. The DNA is encased in the viral core. Two lateral bodies are found outside the viral core, and are believed to hold the enzymes required for viral reproduction. The camelpox virus most often affects members of family Camelidae. However, ...
... s (/ˈfɛzənt/ FEH-zənt) are birds of several genera within the family Phasianidae in the order Galliformes. Although they can be found all over the world in introduced (and captive) populations, the pheasant genera native range is restricted to Eurasia. The classification "pheasant" is paraphyletic, as birds referred to as pheasants are included within both the subfamilies Phasianinae and Pavoninae, and in many cases are more closely related to smaller phasianids, grouse, and turkey (formerly classified in Perdicinae, Tetraoninae, and Meleagridinae) than to other pheasants. Pheasants are characterised by strong sexual dimorphism, males being highly decorated with bright colours and adornments such as wattles. Males are usually larger than females and have longer tails. Males play no part in rearing the young. A pheasants call or cry can be recognised due to the fact it sounds like a rusty sink or valve being turned. Pheasants eat mostly seeds, grains, roots, and berries, while in the ...
Paul S. Mischel (born July 13, 1962) is an American physician-scientist whose laboratory has made pioneering discoveries in the pathogenesis of human cancer. He is currently a Professor and Vice Chair of Research for the Department of Pathology and Institute Scholar of ChEM-H, Stanford University. Mischel was elected into the American Society for Clinical Investigation (ASCI), serving as ASCI president in 2010/11. He was inducted into the Association of American Physicians, and was elected as a fellow of the American Association for the Advancement of Science. Mischel was born on July 13, 1962. After losing his father to cancer, he became committed to a career in cancer research. He attended the University of Pennsylvania and received his M.D. from Cornell University Medical College in 1991, graduating Alpha Omega Alpha. Mischel completed residency training in Anatomic Pathology and Neuropathology at UCLA, followed by post-doctoral research training with Louis Reichardt at HHMI-UCSF. Mischel ...
In this study we demonstrate, for the first time, a homozygous mutation in the alpha6 integrin gene (ITGA6) in a family with ... Homozygous alpha6 integrin mutation in junctional epidermolysis bullosa with congenital duodenal atresia L Pulkkinen 1 , V E ... Homozygous alpha6 integrin mutation in junctional epidermolysis bullosa with congenital duodenal atresia L Pulkkinen et al. Hum ... Altered expression of alpha6 integrin, which forms a heterodimer with the beta4 subunit at the dermal-epidermal junction, would ...
Integrin alpha6 / analysis Actions. * Search in PubMed * Search in MeSH * Add to Search ...
MeSH Terms: Cell Adhesion; Cell Line, Tumor; Cell Movement*; Humans; Integrin alpha6/metabolism*; Integrin beta1/metabolism*; ... Site-specific S-nitrosylation of integrin α6 increases the extent of prostate cancer cell migration by enhancing integrin β1 ...
Identification of the human alpha6 integrin gene promoter.. Lin CS; Chen Y; Huynh T; Kramer R. DNA Cell Biol; 1997 Aug; 16(8): ...
VLA and alpha6, beta4 integrins. Expression in normal and neoplastic human tissues].. Hofman P; Colas P; Manie S; Beck A; ... Integrin-mediated laminin-1 adhesion upregulates CXCR4 and IL-8 expression in pancreatic cancer cells.. Grzesiak JJ; Smith KC; ... Alteration of integrin expression by glial cell line-derived neurotrophic factor (GDNF) in human pancreatic cancer cells. ... The role of NFAT transcription factors in integrin-mediated carcinoma invasion.. Jauliac S; López-Rodriguez C; Shaw LM; Brown ...
... of two proteins known as α6β4 integrin and α6β1 integrin. Learn about this gene and related health conditions. ... Contributions of the alpha6 integrins to breast carcinoma survival and progression. Mol Cells. 2004 Apr 30;17(2):203-9. ... of two proteins known as α6β4 integrin and α6β1 integrin. Integrins are a group of proteins that regulate the attachment of ... Allegra M, Gagnoux-Palacios L, Gache Y, Roques S, Lestringant G, Ortonne JP, Meneguzzi G. Rapid decay of alpha6 integrin caused ...
Integrin alpha6A Integrin alpha6B alpha(6) Integrin alpha6 Integrin Registry Number. 0. Previous Indexing. Antigens, CD (1994- ... Integrin alpha6beta1. Integrin alpha6beta4. Public MeSH Note. 2003; INTEGRIN ALPHA6 was indexed under ANTIGENS, CD 1994-2002. ... Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their ... Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their ...
CRYSTAL STRUCTURE OF A TANDEM PAIR OF FIBRONECTIN TYPE III DOMAINS FROM THE CYTOPLASMIC TAIL OF INTEGRIN ALPHA6 BETA4. ... Integrin AlphaVBeta3 ectodomain bound to the tenth domain of Fibronectin. 4mmy. Integrin AlphaVBeta3 ectodomain bound to the ... Integrin AlphaVBeta3 ectodomain bound to an antagonistic tenth domain of Fibronectin. 4n5u. Crystal structure of the 4th FN3 ... Crystal structure of a complex between integrin beta4 and plectin. 3f7q. First pair of Fibronectin type III domains and part of ...
... non-tumorigenic MCF 10A breast epithelial spheroids should appear round with a hollow center with Integrin alpha-6 polarized to ...
Integrin alpha6A. Integrin alpha6B. Integrin, alpha6. alpha(6) Integrin. alpha6 Integrin. alpha6, Integrin. alpha6A, Integrin. ... Integrin alpha6 Entry term(s). Antigen, CD49f Antigens, CD49f CD49f Antigen CD49f Antigens Integrin, alpha6 alpha(6) Integrin ... Integrin alpha6 - Preferred Concept UI. M0237213. Scope note. An integrin alpha subunit that primarily associates with INTEGRIN ... Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their ...
Integrin alpha6A Integrin alpha6B alpha(6) Integrin alpha6 Integrin Registry Number. 0. Previous Indexing. Antigens, CD (1994- ... Integrin alpha6beta1. Integrin alpha6beta4. Public MeSH Note. 2003; INTEGRIN ALPHA6 was indexed under ANTIGENS, CD 1994-2002. ... Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their ... Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their ...
RADIATION SIGNALING THROUGH THE ALPHA6 BETA 4 INTEGRIN. Cress, A. E.. Project: Research project ... Human Prostate Cancer Metastasis and Laminin Binding Integrins. Cress, A. E. & Cress, A. E. ...
Alpha-6 integrin is necessary for the tumourigenicity of a stem cell-like subpopulation within the MCF7 breast cancer cell line ...
The alpha 6 beta 4 integrin may promote tumorigenesis, while the alpha 6 beta 1 integrin may negatively regulate erbB2/HER2 ... Integrin alpha-6/beta-1 (ITGA6:ITGB1) is present in oocytes and is involved in sperm-egg fusion (By similarity). Integrin alpha ... The gene encodes a member of the integrin alpha chain family of proteins. Integrins are heterodimeric integral membrane ... This subunit may associate with a beta 1 or beta 4 subunit to form an integrin that interacts with extracellular matrix ...
Promotes cell adhesion and adhesive signaling through integrin alpha-6/beta-1, cell migration through integrin alpha-v/beta-5 ... PAI-1 and integrins alpha-3 and alpha-5. CYR61-mediated gene regulation is dependent on heparin-binding. Down-regulates the ...
alpha6-beta4 integrin-Fyn complex GO:0071098 * alphaIIb-beta3 integrin-CD47-FAK complex ...
Purchase Recombinant Human Integrin beta-4(ITGB4),Yeast,partial,Yeast. It is produced in Yeast. High purity. Good price. ... Integrin alpha-6/beta-4 is a receptor for laminin. Plays a critical structural role in the hemidesmosome of epithelial cells. ... Integrin alpha-6/beta-4 is predominantly expressed by epithelia. Isoform beta-4D is also expressed in colon and placenta. ... Recombinant Human Integrin beta-4(ITGB4),partial ( E.coli-CSB-EP011887HU3 ). *Recombinant Human Integrin beta-4(ITGB4), ...
Integrin alpha6 maintains the structural integrity of the kidney collecting system. Matrix Biol. 2017;57-58:244-257.. View this ... Of the 24 known α-β integrin heterodimers, 12 integrins contain the β1 subunit. β1 Integrins are present in epithelial cells, ... β1 Integrin is deleted in type 2 AECs in β1rtTA lungs. (A) Immunostaining for pro-SP-C (green) and β1 integrin (red) ... De Arcangelis A, Mark M, Kreidberg J, Sorokin L, Georges-Labouesse E. Synergistic activities of alpha3 and alpha6 integrins are ...
These cells showed delayed proliferation, inhibited motility and decreased expression of integrin alpha6 and consequently ... and blocking experiments confirmed that it could be attributed to decreased expression of integrin alpha6. The present results ... This effect was independent of beta1-integrins expression CONCLUSION: In addition to inhibition of cancer cell growth, ...
Expression of the 67 kDa laminin receptor and the alpha6 integrin subunit in serous ovarian carcinoma. Clin Exp Metastasis, 20 ... Alphav integrin expression is a novel marker of poor prognosis in advanced-stage ovarian carcinoma. Clin Cancer Res, 7 (12), ... Quantitative analysis of integrin expression in effusions using flow cytometric immunophenotyping. Diagn Cytopathol, 33 (5), ... AlphaV- and beta1-integrin subunits are commonly expressed in malignant effusions from ovarian carcinoma patients. Gynecol ...
... analysis showed expression of integrin alpha6 chain on most CD34(+) and CD34(+)CD38(-) cells. ... JCI - Targeting VLA4 integrin and CXCR2 mobilizes serially repopulating hematopoietic stem cells. Downloading a figure as ... JCI - Targeting VLA4 integrin and CXCR2 mobilizes serially repopulating hematopoietic stem cells. Downloading a figure as ... Laminins are alphabetagamma heterotrimeric extracellular proteins that regulate cellular functions by adhesion to integrin and ...
Integrin alpha-6 is a protein that in humans is encoded by the ITGA6 gene.-Interactions:ITGA6 has been shown to interact with ... Integrin alpha4beta1 is an integrin dimer. It is composed of CD49d and CD29 .VCAM-1 binds to the integrin VLA-4 which are ... Integrin alpha M. Integrin alpha M is one protein subunit that forms the heterodimeric integrin alpha-M beta-2 molecule, also ... αVβ3 is a type of integrin that is a receptor for vitronectin. It consists of two components, integrin alpha V and integrin ...
1. The extracellular endings of a.) alpha6-beta4-Integrins of hemidesosomes, b.) cell surface receptor proteins (CD 44 - ... or Fibronectin which is bound to the alpha subunit of integrins (c). Further molecules reach from the cell membrane into the ... receptor and lamininreceptors) and c.) integrins of adhesion plaques (Areae densae of smooth muscle cells) to which anchoring ...
Am J Med Genet 39:380-384 Pulkkinen L, Kimonis VE, Xu Y, Spanou EN, McLean WH, Uitto J (1997) Homozygous alpha6 integrin ...
Developmentally regulated expression of integrin alpha-6 distinguishes neural crest derivatives in the skin https://pubmed.ncbi ...
N0000171340 Integrin alpha4beta1 N0000171291 Integrin alpha5 N0000169187 Integrin alpha5beta1 N0000171262 Integrin alpha6 ... N0000169180 Integrin alpha6beta1 N0000168758 Integrin alpha6beta4 N0000171277 Integrin alphaV N0000169186 Integrin alphaVbeta3 ... N0000171067 Integrin alphaXbeta2 N0000168744 Integrin beta Chains N0000171315 Integrin beta3 N0000171286 Integrin beta4 ... Factors N0000168743 Integrin alpha Chains N0000171303 Integrin alpha1 N0000168872 Integrin alpha1beta1 N0000171281 Integrin ...
Integrin cell surface interactions (Homo sapiens) * Collagen type IV binds integrin alpha10beta1 (Homo sapiens) * Collagen IV [ ... Tropocollagen alpha-1(IV).alpha-2(IV).alpha-5(IV).alpha-6(IV) [extracellular region] (Homo sapiens) * Collagen alpha-6(IV) ... Tropocollagen alpha-1(IV).alpha-2(IV).alpha-5(IV).alpha-6(IV) [extracellular region] (Homo sapiens) * Collagen alpha-6(IV) ... Tropocollagen alpha-1(IV).alpha-2(IV).alpha-5(IV).alpha-6(IV) [extracellular region] (Homo sapiens) * Collagen alpha-6(IV) ...
Integrin alpha5 D23.50.301.264.35.293 D23.50.301.264.35.354 D23.101.100.110.294 D23.101.100.110.354 Integrin alpha6 D23.50. ... Integrin beta3 D23.50.301.264.35.302 D23.50.301.264.35.357 D23.101.100.110.299 D23.101.100.110.357 Integrin beta4 D23.50. ... Integrin alpha1beta1 D12.776.543.750.70.100 D12.776.543.750.685.100 Integrin alpha2 D23.50.301.264.35.288 D23.50.301.264.35.351 ... Integrin alpha3beta1 D12.776.543.750.70.300 D12.776.543.750.685.300 Integrin alpha4 D23.50.301.264.35.291 D23.50.301.264.35.353 ...
  • These anchoring structures are ultrastructurally abnormal in patients affected with junctional epidermolysis bullosa with pyloric atresia (PA-JEB), a recessively inherited blistering disease of skin and mucosae characterized by an altered immunoreactivity with antibodies specific to integrin alpha6beta4. (nih.gov)
  • Allegra M, Gagnoux-Palacios L, Gache Y, Roques S, Lestringant G, Ortonne JP, Meneguzzi G. Rapid decay of alpha6 integrin caused by a mis-sense mutation in the propeller domain results in severe junctional epidermolysis bullosa with pyloric atresia. (medlineplus.gov)
  • Alpha 6 beta 4 integrin abnormalities in junctional epidermolysis bullosa with pyloric atresia. (medlineplus.gov)
  • Gache Y, Romero-Graillet C, Spadafora A, Lepinard C, Descamps P, Bardon CB, Ortonne JP, Meneguzzi G. A novel homozygous mutation affecting integrin alpha6 in a case of junctional epidermolysis bullosa with pyloric atresia detected in utero by ultrasound examination. (medlineplus.gov)
  • The gene encodes a member of the integrin alpha chain family of proteins. (nih.gov)
  • Integrins are heterodimeric integral membrane proteins composed of an alpha chain and a beta chain that function in cell surface adhesion and signaling. (nih.gov)
  • This subunit may associate with a beta 1 or beta 4 subunit to form an integrin that interacts with extracellular matrix proteins including members of the laminin family. (nih.gov)
  • The ITGA6 gene provides instructions for making one part (the α6 subunit) of two proteins known as α6β4 integrin and α6β1 integrin. (medlineplus.gov)
  • Integrins are a group of proteins that regulate the attachment of cells to one another (cell-cell adhesion) and to the surrounding network of proteins and other molecules (cell-matrix adhesion). (medlineplus.gov)
  • As part of a complex network of proteins in hemidesmosomes, α6β4 integrin helps to hold the layers of skin together. (medlineplus.gov)
  • The integrin proteins activate key signaling molecules, which trigger cancer cells to migrate through the body and invade other tissues. (medlineplus.gov)
  • The alpha6 integrin subunit participates in the formation of both alpha6beta1 and alpha6beta4 laminin receptors, which have been reported to play an important role in cell adhesion and migration and in morphogenesis. (nih.gov)
  • Chung J, Yoon S, Datta K, Bachelder RE, Mercurio AM. Hypoxia-induced vascular endothelial growth factor transcription and protection from apoptosis are dependent on alpha6beta1 integrin in breast carcinoma cells. (medlineplus.gov)
  • In this report, we describe the first mutation in the alpha6 integrin gene in a PA-JEB patient presenting with generalized skin blistering, aplasia cutis, and defective expression of integrin alpha6beta4. (nih.gov)
  • 32. Identification of the human alpha6 integrin gene promoter. (nih.gov)
  • The ITGA6 gene mutations responsible for EB-PA lead to a loss of functional α6β4 integrin. (medlineplus.gov)
  • Integrin alpha-6/beta-1 (ITGA6:ITGB1) is a receptor for laminin on platelets (By similarity). (nih.gov)
  • Integrin alpha-6/beta-1 (ITGA6:ITGB1) is present in oocytes and is involved in sperm-egg fusion (By similarity). (nih.gov)
  • Integrin alpha-6/beta-4 (ITGA6:ITGB4) is a receptor for laminin in epithelial cells and it plays a critical structural role in the hemidesmosome (By similarity). (nih.gov)
  • Integrin alpha6 has two alternatively spliced isoforms: integrin alpha6A and integrin alpha6B, which differ in their cytoplasmic domains and are regulated in a tissue-specific and developmental stage-specific manner. (nih.gov)
  • Site-specific S-nitrosylation of integrin α6 increases the extent of prostate cancer cell migration by enhancing integrin β1 association and weakening adherence to laminin-1. (nih.gov)
  • An integrin alpha subunit that primarily associates with INTEGRIN BETA1 or INTEGRIN BETA4 to form laminin-binding heterodimers. (nih.gov)
  • Integrin alpha-6/beta-4 is a receptor for laminin. (cusabio.com)
  • Expression levels of genes encoding keratin 14, keratin 5, integrin alpha6, integrin beta4, collagen VII, and laminin 5 in these cells were similar to those in basal keratinocytes. (qima-lifesciences.com)
  • Integrin α6A (ITGA6A)-type Splice Variant in Extracellular Vesicles Has a Potential as a Novel Marker of the Early Recurrence of Pancreatic Cancer. (nih.gov)
  • Pancreatic ductal adenocarcinoma cells employ integrin α6β4 to form hemidesmosomes and regulate cell proliferation. (nih.gov)
  • MUC5AC interacts with integrin beta4 that mediates phosphorylation of FAK at Y397 leading to lung cancer cell migration. (cusabio.com)
  • An unusually small rotation between domains 9 and 10 creates a distinctive binding site, in which the RGD loop from domain 10 and the "synergy" region from domain 9 are on the same face of FN7-10 and thus easily accessible to a single integrin molecule. (embl.de)
  • The α6β4 integrin protein is found primarily in epithelial cells, which are cells that line the surfaces and cavities of the body. (medlineplus.gov)
  • The α6β1 integrin protein has not been as well studied as α6β4 integrin. (medlineplus.gov)
  • Integrins also transmit chemical signals that regulate cell growth and the activity of certain genes. (medlineplus.gov)
  • Researchers believe that both α6β1 integrin and α6β4 integrin may play critical roles in the progression of cancerous tumors called carcinomas. (medlineplus.gov)
  • Changes in the location and activity of α6β1 integrin and α6β4 integrin within cancer cells are associated with the progression of carcinomas. (medlineplus.gov)
  • Recent studies suggest that, in addition to their roles in the progression of existing carcinomas, α6β1 integrin and α6β4 integrin may be involved in the initial formation of these tumors. (medlineplus.gov)
  • Chung J, Mercurio AM. Contributions of the alpha6 integrins to breast carcinoma survival and progression. (medlineplus.gov)
  • These findings suggest that the integrin beta4-FAK/Src signaling axis may play a crucial role in clonorchiasis-associated cholangiocarcinoma metastasis during tumor progression. (cusabio.com)
  • The resulting shortage of functional α6β4 integrin causes cells in the epidermis to be fragile and easily damaged. (medlineplus.gov)
  • The alpha 6 beta 4 integrin may promote tumorigenesis, while the alpha 6 beta 1 integrin may negatively regulate erbB2/HER2 signaling. (nih.gov)
  • These mutations alter the normal structure and function of the α6 integrin subunit or prevent cells from producing enough of this subunit. (medlineplus.gov)
  • There are many types of integrin, and many cells have multiple types on their surface. (absoluteastronomy.com)
  • Our results demonstrate that, despite the widespread distribution of the alpha6 integrin subunit, lack of expression of the alpha6 integrin chain is compatible with fetal development, and results in a phenotype indistinguishable from that caused by mutations in the beta4 chain, which is expressed in a more limited number of tissues. (nih.gov)
  • This work investigates alpha6beta4 integrin genetic variations (A380T and R1281W) and breast cancer risk in an Argentinian population. (cusabio.com)
  • The other integrin made with the α6 subunit, α6β1 integrin, functions during the formation of organs and tissues before birth. (medlineplus.gov)
  • The mutation (791delC) is a homozygous deletion of a single base (C) leading to a frameshift and a premature termination codon that results in a complete absence of alpha6 polypeptide. (nih.gov)
  • Altered expression of alpha6 integrin, which forms a heterodimer with the beta4 subunit at the dermal-epidermal junction, would explain fragility and blistering as a result of minor trauma to the skin. (nih.gov)
  • The ITGA6 gene provides instructions for making one part (the α6 subunit) of two proteins known as α6β4 integrin and α6β1 integrin. (medlineplus.gov)
  • The other integrin made with the α6 subunit, α6β1 integrin, functions during the formation of organs and tissues before birth. (medlineplus.gov)
  • These mutations alter the normal structure and function of the α6 integrin subunit or prevent cells from producing enough of this subunit. (medlineplus.gov)
  • 15. Selective down-regulation of the alpha6-integrin subunit in melanocytes by UVB light. (nih.gov)
  • The beta-4 integrin subunit performs a central role in hemidesmosome formation and contains an especially large cytoplasmic domain, which interacts with other proteins of the hemidesmosomal plaque. (medscape.com)
  • An integrin alpha subunit that primarily associates with INTEGRIN BETA1 or INTEGRIN BETA4 to form laminin-binding heterodimers. (nih.gov)
  • Genomic organization of the integrin beta 4 gene (ITGB4): a homozygous splice-site mutation in a patient with junctional epidermolysis bullosa associated with pyloric atresia. (nih.gov)
  • Allegra M, Gagnoux-Palacios L, Gache Y, Roques S, Lestringant G, Ortonne JP, Meneguzzi G. Rapid decay of alpha6 integrin caused by a mis-sense mutation in the propeller domain results in severe junctional epidermolysis bullosa with pyloric atresia. (medlineplus.gov)
  • Alpha 6 beta 4 integrin abnormalities in junctional epidermolysis bullosa with pyloric atresia. (medlineplus.gov)
  • Gache Y, Romero-Graillet C, Spadafora A, Lepinard C, Descamps P, Bardon CB, Ortonne JP, Meneguzzi G. A novel homozygous mutation affecting integrin alpha6 in a case of junctional epidermolysis bullosa with pyloric atresia detected in utero by ultrasound examination. (medlineplus.gov)
  • In this study we demonstrate, for the first time, a homozygous mutation in the alpha6 integrin gene (ITGA6) in a family with three affected individuals. (nih.gov)
  • Hemidesmosomes also contain the intracellular portions of the transmembrane proteins collagen XVII (BP180) and alpha-6-beta-4 integrin. (medscape.com)
  • These structures contain the extracellular portions of collagen XVII (BP180) and alpha-6-beta-4 integrin. (medscape.com)
  • 14. Integrin laminin receptor profile of pulmonary squamous cell and adenocarcinomas. (nih.gov)
  • La integrina alfa6beta4 también se encuentra en los timocitos, fibroblastos y células de Schwann, dónde funciona como receptor de laminina (RECEPTORES DE LAMININA) y está implicada en la cicatrización de heridas, la migración celular y la invasividad tumoral. (bvsalud.org)
  • Integrin alpha6beta4 is also found on thymocytes, fibroblasts, and Schwann cells, where it functions as a laminin receptor (RECEPTORS, LAMININ) and is involved in wound healing, cell migration, and tumor invasiveness. (bvsalud.org)
  • 5. Different phenotypes in human prostate cancer: alpha6 or alpha3 integrin in cell-extracellular adhesion sites. (nih.gov)
  • 9. Integrin clipping: a novel adhesion switch? (nih.gov)
  • 10. Tetraspanin CD82 attenuates cellular morphogenesis through down-regulating integrin alpha6-mediated cell adhesion. (nih.gov)
  • Integrins also transmit chemical signals that regulate cell growth and the activity of certain genes. (medlineplus.gov)
  • 12. α integrin targeting for radiosensitization of three-dimensionally grown human head and neck squamous cell carcinoma cells. (nih.gov)