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.
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.
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.
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 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.
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 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.
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 alpha subunit that binds COLLAGEN and LAMININ though its I domain. It combines with INTEGRIN BETA1 to form the heterodimer INTEGRIN ALPHA1BETA1.
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 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.
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.
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.
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.
Adherence of cells to surfaces or to other cells.
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.
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 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)
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.
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.
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.
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.
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.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
The 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.
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.
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.
An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.
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 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)
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).
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 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)
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Tetraspanin proteins found associated with LAMININ-binding INTEGRINS. The CD151 antigens may play a role in the regulation of CELL MOTILITY.
Established cell cultures that have the potential to propagate indefinitely.
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 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.
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.
Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.
The process whereby PLATELETS adhere to something other than platelets, e.g., COLLAGEN; BASEMENT MEMBRANE; MICROFIBRILS; or other "foreign" surfaces.
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.
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.
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.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Antibodies produced by a single clone of cells.
Proteins prepared by recombinant DNA technology.
An 11-kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
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.
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.
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 cell line derived from cultured tumor cells.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A family of non-receptor, PROLINE-rich protein-tyrosine kinases.
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.
Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A 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.
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.
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.
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.
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.
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.
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
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.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
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).
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.
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.
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.
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).
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.
The rate dynamics in chemical or physical systems.
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.
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.
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.
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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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)
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
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.
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.
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.
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).
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.
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.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
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).
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.
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)
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.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm.
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.
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.
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.
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.
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.
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.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
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.
Protein kinases that catalyze the PHOSPHORYLATION of TYROSINE residues in proteins with ATP or other nucleotides as phosphate donors.
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.
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.
Elements of limited time intervals, contributing to particular results or situations.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
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.
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.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
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.
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.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
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.
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.
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.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
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.
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 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 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.
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.
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.
The process by which two molecules of the same chemical composition form a condensation product or polymer.
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.
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.
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.
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.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
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.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Glycoproteins found on the membrane or surface of cells.
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.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
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.
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.
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.
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.
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.
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 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.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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).
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.
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.
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 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.
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.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
A dynamic actin-rich extension of the surface of an animal cell used for locomotion or prehension of food.
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.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
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.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
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.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
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)
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
A 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.
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.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
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.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Sites on an antigen that interact with specific antibodies.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A 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.
A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.
Positively charged atoms, radicals or groups of atoms with a valence of plus 2, which travel to the cathode or negative pole during electrolysis.
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)

Distinct functions of alpha3 and alpha(v) integrin receptors in neuronal migration and laminar organization of the cerebral cortex. (1/258)

Changes in specific cell-cell recognition and adhesion interactions between neurons and radial glial cells regulate neuronal migration as well as the establishment of distinct layers in the developing cerebral cortex. Here, we show that alpha3beta1 integrin is necessary for neuron-glial recognition during neuronal migration and that alpha(v) integrins provide optimal levels of the basic neuron-glial adhesion needed to maintain neuronal migration on radial glial fibers. A gliophilic-to-neurophilic switch in the adhesive preference of developing cortical neurons occurs following the loss of alpha3beta1 integrin function. Furthermore, the targeted mutation of the alpha3 integrin gene results in abnormal layering of the cerebral cortex. These results suggest that alpha3beta1 and alpha(v) integrins regulate distinct aspects of neuronal migration and neuron-glial interactions during corticogenesis.  (+info)

Pro-adhesive and chemotactic activities of thrombospondin-1 for breast carcinoma cells are mediated by alpha3beta1 integrin and regulated by insulin-like growth factor-1 and CD98. (2/258)

Thrombospondin-1 (TSP1) is a matricellular protein that displays both pro- and anti-adhesive activities. Binding to sulfated glycoconjugates mediates most high affinity binding of soluble TSP1 to MDA-MB-435 cells, but attachment and spreading of these cells on immobilized TSP1 is primarily beta1 integrin-dependent. The integrin alpha3beta1 is the major mediator of breast carcinoma cell adhesion and chemotaxis to TSP1. This integrin is partially active in MDA-MB-435 cells but is mostly inactive in MDA-MB-231 and MCF-7 cells, which require beta1 integrin activation to induce spreading on TSP1. Integrin-mediated cell spreading on TSP1 is accompanied by extension of filopodia containing beta1 integrins. TSP1 binding activity of the alpha3beta1 integrin is not stimulated by CD47-binding peptides from TSP1 or by protein kinase C activation, which activate alphavbeta3 integrin function in the same cells. In MDA-MB-231 but not MDA-MB-435 cells, this integrin is activated by pertussis toxin, whereas serum, insulin, insulin-like growth factor-1, and ligation of CD98 increase activity of this integrin in both cell lines. Serum stimulation is accompanied by increased surface expression of CD98, whereas insulin-like growth factor-1 does not increase CD98 expression. Thus, the pro-adhesive activity of TSP1 for breast carcinoma cells is controlled by several signals that regulate activity of the alpha3beta1 integrin.  (+info)

Ligand-specific, transient interaction between integrins and calreticulin during cell adhesion to extracellular matrix proteins is dependent upon phosphorylation/dephosphorylation events. (3/258)

As transmembrane heterodimers, integrins bind to both extracellular ligands and intracellular proteins. We are currently investigating the interaction between integrins and the intracellular protein calreticulin. A prostatic carcinoma cell line (PC-3) was used to demonstrate that calreticulin can be found in the alpha3 immunoprecipitates of cells plated on collagen type IV, but not when plated on vitronectin. Conversely, alphav immunoprecipitates contained calreticulin only when cells were plated on vitronectin, i. e. not when plated on collagen IV. The interactions between these integrins and calreticulin were independent of actin cytoskeleton assembly and were transient, being maximal approx. 10-30 min after the cells came into contact with the substrates prior to complete cell spreading and formation of firm adhesive contacts. We demonstrate that okadaic acid, an inhibitor of intracellular serine/threonine protein phosphatases, inhibited the alpha3beta1-mediated adhesion of PC-3 cells to collagen IV and the alpha2beta1-mediated attachment of Jurkat cells to collagen I. This inhibition by okadaic acid was accompanied by inhibition of the ligand-specific interaction of calreticulin with the respective integrins in the two cell types. Additionally, we found that pharmacological inhibition of mitogen-activated protein kinase kinase (MEK) resulted in prolongation of the calreticulin-integrin interaction, and enhancement of PC-3 cell attachment to collagen IV. We conclude that calreticulin interacts transiently with integrins during cell attachment and spreading. This interaction depends on receptor occupation, is ligand-specific, and can be modulated by protein phosphatase and MEK activity.  (+info)

Selective tetraspan-integrin complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions. (4/258)

The tetraspans are molecules with four transmembrane domains which are engaged in multimolecular complexes (the tetraspan web) containing a subset of beta1 integrins (in particular alpha3beta1, alpha4beta1 and alpha6beta1), MHC antigens and several unidentified molecules. The molecules associated with tetraspans are readily detected after immunoprecipitation performed in mild detergents such as Brij 97 or CHAPS. In this study we show that another classical mild detergent, digitonin, dissociated most of these associated molecules, including integrins, from the tetraspans CD9, CD37, CD53, CD63, CD82, Co-029, Talla-1 and NAG-2. In contrast, reciprocal immunoprecipitations from various cell lines demonstrated that two other tetraspans, CD81 and CD151, formed complexes with integrins not disrupted by digitonin. These complexes were CD81/alpha4beta1, CD151/alpha3beta1 and CD151/alpha6beta1. Furthermore, a new anti-CD151 monoclonal antibody (mAb), TS151r, was shown to have a restricted pattern of expression, inversely related to the sum of the levels of expression of alpha6beta1 and alpha3beta1. This mAb was unable to co-precipitate integrins in digitonin, suggesting that its epitope is blocked by the association with integrins. Indeed, the binding of TS151r to the cell surface was quantitatively diminished following alpha3beta1 overexpression. Altogether, these data suggest that, among tetraspans, CD81 interacts directly with the integrin alpha4beta1, and CD151 interacts directly with integrins alpha3beta1 and alpha6beta1. Because all tetraspan-tetraspan associations are disrupted by digitonin, it is likely that the other tetraspans interact indirectly with integrins, through interactions with CD81 or CD151.  (+info)

An IKLLI-containing peptide derived from the laminin alpha1 chain mediating heparin-binding, cell adhesion, neurite outgrowth and proliferation, represents a binding site for integrin alpha3beta1 and heparan sulphate proteoglycan. (5/258)

We synthesized and characterized several peptides containing the IKLLI sequence in the alpha1 chain of laminin-1. The IKLLI-containing peptides, such as LA4 (CSRNLSEIKLLISRARK), LA5 (EIKLLIS) and LA5L (SEIKLLIS), were found to mediate heparin binding and cell adhesion, while also promoting neurite outgrowth in PC12 cells. Furthermore, peptides LA4 and LA5 also mediated proliferation. However, a scrambled peptide, LA5S (ILEKSLI), did not show any of these activities. Anti-LA4 antibodies inhibited laminin- and LA5-mediated cell adhesion and neurite outgrowth, and anti-(integrin alpha3) and anti-(integrin beta1) antibodies inhibited LA5-mediated cell adhesion and neurite outgrowth. Heparin and heparan sulphate inhibited LA5-mediated heparin binding and PC12 cell adhesion in a dose- dependent manner. The IC50 for inhibition of heparin binding and cell adhesion was observed with 9 microM and 8 microM heparin/heparan sulphate respectively. Furthermore, heparan sulphate proteoglycan also inhibited LA5-mediated PC12 cell adhesion with an IC50 of 100 micrograms/ml. However, chondroitin sulphate (dermatan sulphate) did not inhibit cell adhesion. These data suggest that an IKLLI-containing peptide derived from the laminin alpha1 chain may be an active site of laminin and that its cell adhesion may thus interact with both integrin alpha3beta1 and cell- surface heparan sulphate proteoglycan.  (+info)

Complement-mediated injury reversibly disrupts glomerular epithelial cell actin microfilaments and focal adhesions. (6/258)

BACKGROUND: Foot process effacement and condensation of the glomerular epithelial cell (GEC) cytoskeleton are manifestations of passive Heymann nephritis, a model of complement-mediated membranous nephropathy. METHODS: To study the effects of complement on the actin cytoskeleton in this model, we have used an in vitro system in which GECs are sublethally injured using a combination of complement-fixing anti-Fx1A IgG and human serum as a source of complement. We examined the effects of this injury on the organization of the cytoskeleton and focal contacts using immunohistology and immunochemistry. RESULTS: By immunofluorescence, sublethal complement-mediated injury was accompanied by a loss of actin stress fibers and focal contacts but retention of matrix-associated integrins. Full recovery was seen after 18 hours. Western blot analysis showed no change in the cellular content of the focal contact proteins. Inhibition of the calcium-dependent protease calpain did not prevent injury. In addition, cycloheximide during recovery did not inhibit the reassembly of stress fibers or focal contacts. Injury was associated with a reduction in tyrosine phosphorylation of paxillin and a currently unidentified 200 kDa protein, but inhibition of tyrosine phosphatase activity with sodium vanadate did not prevent injury. Cellular adenosine triphosphate content was significantly reduced in injured cells. CONCLUSION: These results document reversible, complement-dependent disruption of actin microfilaments and focal contacts leading to the dissociation of the cytoskeleton from matrix-attached integrins. This may explain the altered cell-matrix relationship accompanying podocyte effacement in membranous nephropathy.  (+info)

Overexpressed alpha3beta1 and constitutively activated extracellular signal-regulated kinase modulate the angiogenic properties of ECV304 cells. (7/258)

ECV304, a spontaneously transformed cell line derived from the human umbilical vein endothelial cell (HUVEC) (Takahashi et al., 1990), has been developed as an in vitro angiogenesis model. In the present study, we further characterized the angiogenic properties of this cell line. Compared to HUVEC, ECV304 cells showed distinct features including a higher activity of cellular adhesion, slower but reproducible progression of angiogenesis on Matrigel, and resistance to apoptosis. Thus, the expression of integrin and activation of extracellular-signal regulated kinase 1/2 (Erk1/2), a downstream effector of the integrin pathway, were examined. Flow cytometry revealed that alpha3beta1 integrin was markedly upregulated in ECV304 cells, while alpha(v)beta1 and alpha5beta1 integrins were slightly downregulated. Consistent with this, the binding activity to collagen type IV and laminin, major extracellular matrices of Matrigel, was increased 1.4- and 1.9-fold in ECV304 cells, respectively. This tight binding may retard the initial stage of sprouting and migration in the angiogenesis of ECV304 cells. It has been further demonstrated that Erk1/2 is constitutively active in ECV304 cells, rendering them resistent to the inhibitory effect of PD98059 on proliferation. However, migration of both HUVEC and ECV304 cells was inhibited to a similar extent by PD98059 in a dose-dependent manner. Up to 50 microM of PD98059, no significant changes in cell binding and tubulogenesis on Matrigel was observed in ECV304 cells. In contrast, the tubulogenesis of HUVEC was severely impaired by PD98059. Elevated Erk1/2 activity in ECV304 cells was suppressed by dominant negative H-Ras, but not by cytochalasin D. These results suggest that the overexpression of alpha3beta1 integrin and the constitutive activation of Erk1/2 play a key role in the alteration of the angiogenic properties of ECV304 cells.  (+info)

The alpha3 laminin subunit, alpha6beta4 and alpha3beta1 integrin coordinately regulate wound healing in cultured epithelial cells and in the skin. (8/258)

Previously, we demonstrated that proteolytic processing within the globular domain of the alpha3 subunit of laminin-5 (LN5) converts LN5 from a cell motility-inducing factor to a protein complex that can trigger the formation of hemidesmosomes, certain cell-matrix attachment sites found in epithelial cells. We have prepared a monoclonal antibody (12C4) whose epitope is located toward the carboxy terminus of the globular domain of the alpha3 laminin subunit. This epitope is lost from the alpha3 subunit as a consequence of proteolytic processing. Antibody 12C4 stains throughout the matrix of cells that fail to process the alpha3 laminin subunit, but does not recognize the matrix of confluent cultures of MCF-10A cells, which efficiently process their alpha3 laminin chain. In subconfluent populations of MCF-10A cells, 12C4 only stains matrix deposited at the outer edges of cell colonies. In these cells, integrin alpha3beta1 occasionally colocalizes with the staining generated by the 12C4 antibody but alpha6beta4 integrin does not. In wounded MCF-10A cell cultures, the 12C4 antibody stains the extracellular matrix beneath those cells at the very edge of the cellular sheet that moves to cover the wound site. A similar phenomenon is observed in human skin wounds, since we also detect expression of the unprocessed alpha3 laminin subunit at the leading tip of the sheet of epidermal cells that epithelializes skin wounds in vivo. In addition, using alpha3 laminin subunit and integrin function-inhibiting antibodies, we provide evidence that LN5 and its two integrin receptors (alpha6beta4 and alpha3beta1) appear necessary for wound healing to occur in MCF-10A cell culture wounds. We propose a model for healing of wounded epithelial tissues based on these results.  (+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.

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

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

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

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

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

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

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

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

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

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

There are 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.

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.

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.

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.

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.

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.

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 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.

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 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.

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.

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

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

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

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

See also: Cancer, Tumor

Word count: 190

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.

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.

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

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.

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.

The post Definition of 'Carcinoma, Lewis Lung' in the medical field appeared first on Healthy Life Tips.

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.

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.

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%.

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.

* 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.

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.

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.

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.

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.

There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia. Alpha-thalassemia is caused by abnormalities in the production of the alpha-globin chain, which is one of the two chains that make up hemoglobin. Beta-thalassemia is caused by abnormalities in the production of the beta-globin chain.

Thalassemia can cause a range of symptoms, including anemia, fatigue, pale skin, and shortness of breath. In severe cases, it can lead to life-threatening complications such as heart failure, liver failure, and bone deformities. Thalassemia is usually diagnosed through blood tests that measure the levels of hemoglobin and other proteins in the blood.

There is no cure for thalassemia, but treatment can help manage the symptoms and prevent complications. Treatment may include blood transfusions, folic acid supplements, and medications to reduce the severity of anemia. In some cases, bone marrow transplantation may be recommended.

Preventive measures for thalassemia include genetic counseling and testing for individuals who are at risk of inheriting the disorder. Prenatal testing is also available for pregnant women who are carriers of the disorder. In addition, individuals with thalassemia should avoid marriage within their own family or community to reduce the risk of passing on the disorder to their children.

Overall, thalassemia is a serious and inherited blood disorder that can have significant health implications if left untreated. However, with proper treatment and management, individuals with thalassemia can lead fulfilling lives and minimize the risk of complications.

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.

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.

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.

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.

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.




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.

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.

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.

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.

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.

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%.

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.

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.

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.

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

There are several different types of neuroblastoma, including:

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

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

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

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

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

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 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.

There are several types of skin neoplasms, including:

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

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

1999). "Selective tetraspan-integrin complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions ... Evidence that alpha3beta1 complexes with EMMPRIN/basigin/OX47/M6". J. Biol. Chem. 272 (46): 29174-80. doi:10.1074/jbc.272.46. ... Horváth G, Serru V, Clay D, Billard M, Boucheix C, Rubinstein E (Nov 1998). "CD19 is linked to the integrin-associated ... This encoded protein is a cell surface glycoprotein that is known to complex with integrins. This protein appears to promote ...
Evidence that alpha3beta1 complexes with EMMPRIN/basigin/OX47/M6". The Journal of Biological Chemistry. 272 (46): 29174-80. doi ... This encoded protein is a cell surface glycoprotein that is known to complex with integrins. It may function as a blood ... Interactions with CD63 may therefore affect the trafficking and function of β2 integrins. In cell biology, CD63 is often used ... Berditchevski F, Bazzoni G, Hemler ME (July 1995). "Specific association of CD63 with the VLA-3 and VLA-6 integrins". The ...
Evidence that alpha3beta1 complexes with EMMPRIN/basigin/OX47/M6". J. Biol. Chem. 272 (46): 29174-80. doi:10.1074/jbc.272.46. ... Berditchevski F, Chang S, Bodorova J, Hemler ME (1997). "Generation of monoclonal antibodies to integrin-associated proteins. ...
Evidence that alpha3beta1 complexes with EMMPRIN/basigin/OX47/M6". The Journal of Biological Chemistry. 272 (46): 29174-29180. ... Berditchevski F, Chang S, Bodorova J, Hemler ME (November 1997). "Generation of monoclonal antibodies to integrin-associated ... Evidence that alpha3beta1 complexes with EMMPRIN/basigin/OX47/M6". The Journal of Biological Chemistry. 272 (46): 29174-29180. ... Berditchevski F, Chang S, Bodorova J, Hemler ME (November 1997). "Generation of monoclonal antibodies to integrin-associated ...
Regulation of epithelial cell cytokine responses by the alpha3beta1 integrin. Immunology. 108: 204-10. PMID 12562329 DOI: ... Lubin inhibited integrin signalling in epithelial cells and exposed them to proinflammatory cytokines. She found that a3B1 ... "Regulation of epithelial cell cytokine responses by the α3β1 integrin". Immunology. 108 (2): 204-210. doi:10.1046/j.1365- ... integrin signalling may be responsible for suppression of cytokine responses in epithelial cells during inflammation and wound ...
Stipp CS, Kolesnikova TV, Hemler ME (2004). "EWI-2 regulates alpha3beta1 integrin-dependent cell functions on laminin-5". J. ... 2006). "Contrasting effects of EWI proteins, integrins, and protein palmitoylation on cell surface CD9 organization". J. Biol. ... 2004). "EWI-2 modulates lymphocyte integrin alpha4beta1 functions". Blood. 103 (8): 3013-9. doi:10.1182/blood-2003-07-2201. ...
Serru V, Le Naour F, Billard M, Azorsa DO, Lanza F, Boucheix C, Rubinstein E (1999). "Selective tetraspan-integrin complexes ( ... CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions". Biochem. J. 340 (1 ... This encoded protein is a cell surface glycoprotein that is known to complex with integrins and other transmembrane 4 ... It is involved in cellular processes including cell adhesion and may regulate integrin trafficking and/or function. This ...
CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions". The Biochemical Journal. 340 (Pt 1 ... This integrin associates with integrin alpha 1 and integrin alpha 2 to form integrin complexes which function as collagen ... Integrin beta-1 is the most abundant beta-integrin expressed and associates with at least 10 different integrin-alpha subunits ... It also forms dimers with integrin alpha 3 to form integrin receptors for netrin 1 and reelin. These and other integrin beta 1 ...
Serru V, Le Naour F, Billard M, Azorsa DO, Lanza F, Boucheix C, Rubinstein E (May 1999). "Selective tetraspan-integrin ... complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions". The ... CD37 is a cell surface glycoprotein that is known to complex with integrins and other transmembrane 4 superfamily proteins. ... Berditchevski F (December 2001). "Complexes of tetraspanins with integrins: more than meets the eye". Journal of Cell Science. ...
Horváth G, Serru V, Clay D, Billard M, Boucheix C, Rubinstein E (November 1998). "CD19 is linked to the integrin-associated ... CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions". The Biochemical Journal. 340 ( Pt 1 ... Horváth G, Serru V, Clay D, Billard M, Boucheix C, Rubinstein E (November 1998). "CD19 is linked to the integrin-associated ... Serru V, Le Naour F, Billard M, Azorsa DO, Lanza F, Boucheix C, Rubinstein E (May 1999). "Selective tetraspan-integrin ...
This encoded protein is a cell surface glycoprotein that is known to complex with integrins. This gene is expressed in ... CD151/alpha3beta1, CD151/alpha6beta1) under conditions disrupting tetraspan interactions". The Biochemical Journal. 340 ( Pt 1 ... Serru V, Le Naour F, Billard M, Azorsa DO, Lanza F, Boucheix C, Rubinstein E (May 1999). "Selective tetraspan-integrin ... Berditchevski F (December 2001). "Complexes of tetraspanins with integrins: more than meets the eye". Journal of Cell Science. ...
Laminin-8 stimulates cell adhesion and migration through alpha3beta1 and alpha6beta1 integrins". J. Biol. Chem. 276 (20): 17550 ... α3β1 Integrin, and Mitogen-activated Protein Kinase Can Regulate Epithelial Cell Proliferation". Mol. Biol. Cell. 10 (2): 259- ...
1999). "Selective tetraspan-integrin complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions ... It is known to complex with integrins. This gene is associated with X-linked mental retardation and neuropsychiatric diseases ... Berditchevski F (2002). "Complexes of tetraspanins with integrins: more than meets the eye". J. Cell Sci. 114 (Pt 23): 4143-51 ... 2001). "Involvement of alpha3 integrin/tetraspanin complexes in the angiogenic response induced by angiotensin II". FASEB J. 15 ...
1999). "Selective tetraspan-integrin complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions ... 2000). "Direct extracellular contact between integrin alpha(3)beta(1) and TM4SF protein CD151". J. Biol. Chem. 275 (13): 9230-8 ... "Entrez Gene: TSPAN4 tetraspanin 4". Berditchevski F (2002). "Complexes of tetraspanins with integrins: more than meets the eye ... It is known to complex with integrins and other transmembrane 4 superfamily proteins. Alternatively spliced transcript variants ...
Santoro MM, Gaudino G, Marchisio PC (2003). "The MSP receptor regulates alpha6beta4 and alpha3beta1 integrins via 14-3-3 ...
1999). "Selective tetraspan-integrin complexes (CD81/alpha4beta1, CD151/alpha3beta1, CD151/alpha6beta1) under conditions ... This encoded protein is a cell surface glycoprotein that is known to complex with integrins. It contributes to the transduction ... Berditchevski F (2002). "Complexes of tetraspanins with integrins: more than meets the eye". J. Cell Sci. 114 (Pt 23): 4143-51 ... 1996). "Transmembrane-4 superfamily proteins CD81 (TAPA-1), CD82, CD63, and CD53 specifically associated with integrin alpha 4 ...
Santoro MM, Gaudino G, Marchisio PC (2003). "The MSP receptor regulates alpha6beta4 and alpha3beta1 integrins via 14-3-3 ...
"NG2 proteoglycan promotes endothelial cell motility and angiogenesis via engagement of galectin-3 and alpha3beta1 integrin". ... "A role of chondroitin sulfate glycosaminoglycan binding site in alpha4beta1 integrin-mediated melanoma cell adhesion". The ...
2002). "Regulation of melanoma cell migration and invasion by laminin-5 and alpha3beta1 integrin (VLA-3)". Clin. Exp. ... 2008). "Laminin Isoforms Containing the γ3 Chain Are Unable to Bind to Integrins due to the Absence of the Glutamic Acid ... Wilhelmsen K, Litjens SH, Sonnenberg A (2006). "Multiple Functions of the Integrin α6β4 in Epidermal Homeostasis and ... Their adhesion to laminin-5 involves multiple receptors among which is integrin alpha2beta1". J. Cell Sci. 111 (14): 1993-2004 ...
Chattopadhyay N, Wang Z, Ashman LK, Brady-Kalnay SM, Kreidberg JA (2003). "alpha3beta1 integrin-CD151, a component of the ... α3β1 integrin and the tetraspanin CD151 regulate PTPmu gene expression to promote E-cadherin-mediated cell-cell adhesion. In ... Sakamoto Y, Ogita H, Komura H, Takai Y (2008). "Involvement of nectin in inactivation of integrin alpha(v)beta(3) after the ...
2003). "Recognition of the neural chemoattractant Netrin-1 by integrins alpha6beta4 and alpha3beta1 regulates epithelial cell ...
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 ...
... alpha3beta1, and alpha5beta1 integrins in local invasiveness and architectural characteristics". Annals of Diagnostic Pathology ... There is also some research suggesting that α5β1 integrin may participate in the local invasiveness of ameloblastomas. People ...
... where the FAS1 domains mediate cell adhesion through an interaction with alpha3/beta1 integrin; mutation in the FAS1 domains ...
She uncovered new mechanisms by which integrins contribute to cancer, including the first tumour-associated integrin mutation. ... alpha3beta1, but not alpha2beta1, suppresses malignant conversion". Cancer Res. 61 (13): 5248-54. PMID 11431366. Hoste, E; ... Evans, RD; Perkins, VC; Henry, A; Stephens, PE; Robinson, MK; Watt, FM (2003). "A tumor-associated beta 1 integrin mutation ... Owens, DM; Watt, FM (2001). "Influence of beta1 integrins on epidermal squamous cell carcinoma formation in a transgenic mouse ...
"Pro-adhesive and chemotactic activities of thrombospondin-1 for breast carcinoma cells are mediated by alpha3beta1 integrin and ... αv integrins, β1 integrins, syndecan, and integrin-associated protein (IAP or CD47). It also interacts with numerous proteases ... This protein can bind to fibrinogen, fibronectin, laminin, collagens types V and VII and integrins alpha-V/beta-1. This protein ...
Integrin alpha1beta1 Integrin alpha2beta1 Integrin alpha3beta1 VLA-4 - Heterodimer: CD49d / CD29 Alpha-5 beta-1 Integrin ... Integrin alpha2beta1 Integrin alpha4beta1 Integrin alpha5beta1 Leukocyte-adhesion receptor: LFA-1 - Heterodimer: CD11a / CD18 ... Beta subunits B1 B2 B3 B4 B5 B6 B7 B8 Dimers Cytoadhesin receptor Integrin alpha6beta4 Glycoprotein IIb/IIIa - Heterodimer: ... differentiation JAK-STAT signaling pathway TGF beta signaling pathway TLR signalling pathway Cell adhesion molecules Integrins ...
... integrin alpha1beta1 MeSH D12.776.543.750.072.200 - integrin alpha2beta1 MeSH D12.776.543.750.072.300 - integrin alpha3beta1 ... integrin alpha2beta1 MeSH D12.776.543.750.705.876.311 - integrin alpha3beta1 MeSH D12.776.543.750.705.876.374 - integrin ... integrin alpha2beta1 MeSH D12.776.543.750.705.408.850.249 - integrin alpha3beta1 MeSH D12.776.543.750.705.408.850.299 - ... integrin alpha1 MeSH D12.776.543.750.705.408.100.350 - integrin alpha2 MeSH D12.776.543.750.705.408.100.400 - integrin alpha3 ...
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 ...
... alpha3beta1 Integrin; alpha3beta1 Epiligrin Receptor; VLA-. 3; Laminin-. 5 Receptor (alpha3beta1 integrin); Integrin alpha(3) ... Other names alpha3beta1, Integrin; Receptor, alpha3beta1 Epiligrin; Receptor, Epiligrin; Integrin, alpha3beta1; Epiligrin ... Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT ... Two alternatively spliced isoforms of the alpha subunit (INTEGRIN ALPHA3), are differentially expressed in different cell types ...
part_of integrin alpha3-beta1 complex IDA Inferred from Direct Assay. more info ... Int_alpha; Integrin alpha (beta-propellor repeats). pfam08441. Location:462 → 916. Integrin_alpha2; Integrin alpha. ... Int_alpha; Integrin alpha (beta-propellor repeats). pfam08441. Location:327 → 781. Integrin_alpha2; Integrin alpha. ... part_of integrin alpha3-beta1 complex IMP Inferred from Mutant Phenotype. more info ...
Urokinase receptors promote beta1 integrin function through interactions with integrin alpha3beta1.. Wei Y; Eble JA; Wang Z; ... Functional relevance of urinary-type plasminogen activator receptor-alpha3beta1 integrin association in proteinase regulatory ... Convergence of the adhesive and fibrinolytic systems: recognition of urokinase by integrin alpha Mbeta 2 as well as by the ... 5. Critical role of integrin alpha 5 beta 1 in urokinase (uPA)/urokinase receptor (uPAR, CD87) signaling.. Tarui T; Andronicos ...
Integrin alpha(3)beta(1) Laminin-5 Receptor (alpha3beta1 integrin) VLA-3 alpha3beta1 Epiligrin Receptor alpha3beta1 Integrin ... 2003; INTEGRIN ALPHA3BETA1 was indexed under INTEGRINS 1992-2002. History Note. 2003; use INTEGRIN ALPHA3BETA1 (NM) 1992-2002. ... Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT ... Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT ...
alpha3-beta1 integrin-tissue transglutaminase complex alpha5-beta1 integrin-fibronectin-tissue transglutaminase complex ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
Epithelial cell alpha3beta1 integrin links beta-catenin and Smad signaling to promote myofibroblast formation and pulmonary ...
Integrin alpha(3)beta(1) Laminin-5 Receptor (alpha3beta1 integrin) VLA-3 alpha3beta1 Epiligrin Receptor alpha3beta1 Integrin ... 2003; INTEGRIN ALPHA3BETA1 was indexed under INTEGRINS 1992-2002. History Note. 2003; use INTEGRIN ALPHA3BETA1 (NM) 1992-2002. ... Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT ... Integrin alpha3beta1 is the major integrin present in EPITHELIAL CELLS, where it plays a role in the assembly of BASEMENT ...
Receptor, alpha3beta1 Epiligrin VLA-3 alpha3beta1 Epiligrin Receptor alpha3beta1 Integrin alpha3beta1, Integrin ... Receptor, alpha3beta1 Epiligrin. VLA-3. alpha3beta1 Epiligrin Receptor. alpha3beta1 Integrin. alpha3beta1, Integrin. ... 2003; INTEGRIN ALPHA3BETA1 was indexed under INTEGRINS 1992-2002. History Note:. 2003; use INTEGRIN ALPHA3BETA1 (NM) 1992-2002 ... Integrin alpha(3)beta(1) Integrin, alpha3beta1 Laminin-5 Receptor (alpha3beta1 integrin) Receptor, Epiligrin ...
The integrins alpha3beta1 and alpha6beta1 physically and functionally associate with CD36 in human melanoma cells. Requirement ... Expression of the alphavbeta6 integrin promotes migration and invasion in squamous carcinoma cells. Thomas, G J; Lewis, M P; ...
alpha3-beta1 integrin-tissue transglutaminase complex GO:0071092 * alphaPDGFR-PLC-gamma-1-PI3K-SHP-2 complex ...
Loss of alpha3beta1 integrin function results in an altered differentiation program in the mouse submandibular gland. Dev Dyn. ... 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) ... Deletion of core fucosylation on alpha3beta1 integrin down-regulates its functions. J Biol Chem. 2006;281(50):38343-38350. ...
N0000171281 Integrin alpha2 N0000169181 Integrin alpha2beta1 N0000171301 Integrin alpha3 N0000168873 Integrin alpha3beta1 ... N0000171285 Integrin alpha4 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 ...
Mechanical stretch induces reduction in alpha3 beta1 integrins in Glomerular Epithelial Cells in vitro.. https://iris.unito.it/ ... Brizzi MF, Tarone G, Defilippi P. (2012) Extracellular matrix, integrins, and growth factors as tailors of the stem cell niche ...
Mediates adhesion of proximal tubule epithelial cells via integrins alpha3-beta1 and alphaV-beta3. This is a non catalytic ... Mediates adhesion of proximal tubule epithelial cells via integrins alpha3-beta1 and alphaV-beta3. This is a non catalytic ...
Migration and Proliferation through the Interaction with Alpha3Beta1 Integrin. Experimental and Molecular Medicine, 36, 211-219 ... 5. Kim, H.J. and Kim, I.S. (2008) Transforming Growth Factor-Beta-Induced Gene Product, as a Novel Ligand of Integrin ... Cleavage of BIGH3 C-terminus yields integrin ligand peptides that induce BMA in various cell types [8] - [12] [32] . To test ... In a paracrine or autocrine mechanism the peptides induce BMA, presumably involving integrins. Thirdly, an increase in the ...
... and was mediated by TIMP-2 binding to the alpha3 beta1 integrin on the surface of human microvascular endothelial cells. These ... Antagonism of VEGF-A-induced increase in vascular permeability by an integrin α3β1-Shp-1-cAMP/PKA pathway. Blood. 2012;120(24): ... activity with this integrin and an increase in PTP activity associated with variety of RTKs (VEGFR-2, FGFR1a, PDGFR and EGFR). ...
P-ERK and p-AKT were reduced by shRNA targeting integrin α6 and PI3K inhibitor LY294002. Knockdown integrin α6 can inhibit the ... Integrin α6 can mediate the metastasis potential, and can be used as a candidate target for therapy in HCC resulting in ... PI3K inhibitor LY294002 was used to explore the signal pathways of integrin α6 in HCC cells. Western blot and qRT-PCR detection ... The aim of this study is to investigate the effect of short hairpin RNA (shRNA) silencing integrin α6 expression on the ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
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 ... Integrin alpha6 D23.50.301.264.35.296 D23.50.301.264.35.355 D23.101.100.110.297 D23.101.100.110.355 Integrin alphaV 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 ... D23.101.100.110.288 D23.101.100.110.351 Integrin alpha2beta1 D12.776.543.750.70.200 D12.776.543.750.685.200 Integrin alpha3 ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
Cosmology: alpha3beta1; Naugarduko str. Dutch Cycling change Ruben Loendersloot; will offer Urban Engineering Department in ... newsreader in Campbells Soup realist of the outputs has all a excellenceNow of Timmy and Lassie or Donna Reeds integrin book ... A Korean download of the alpha3beta1 is its 2011Received look to the Encountering foregrounding of conditions coding the 2010- ...
Reelin binds alpha3beta1 integrin and inhibits neuronal migration L Dulabon 1 , E C Olson, M G Taglienti, S Eisenhuth, B ... Reelin binds alpha3beta1 integrin and inhibits neuronal migration L Dulabon et al. Neuron. 2000 Jul. ... Recombinant and native Reelin associate with alpha3beta1 integrin, which regulates neuron-glia interactions and is required to ... Thus, Reelin may arrest neuronal migration and promote normal cortical lamination by binding alpha3beta1 integrin and ...
Integrin alpha3beta1/metabolism; Lamins/metabolism*; Leukocyte Elastase/metabolism; Lipopolysaccharides; Lung Neoplasms/ ... The proteolytically remodeled laminin induced proliferation of dormant cancer cells by activating integrin α3β1 signaling. ...
8. Integrin alpha3beta1 engagement disrupts intercellular adhesion.. Kawano K; Kantak SS; Murai M; Yao CC; Kramer RH. Exp Cell ... An all-D amino acid peptide model of alpha1(IV)531-543 from type IV collagen binds the alpha3beta1 integrin and mediates tumor ... ECM dependent and integrin mediated tumor cell migration of human glioma and melanoma cell lines under serum-free conditions. ... 7. Identification of CD47/integrin-associated protein and alpha(v)beta3 as two receptors for the alpha3(IV) chain of type IV ...
Integrin alpha3beta1 engagement disrupts intercellular adhesion. Kawano K, Kantak SS, Murai M, Yao CC, Kramer RH. Kawano K, et ... Receptor binding domain of SARS-CoV-2 is a functional αv-integrin agonist. Norris EG, Pan XS, Hocking DC. Norris EG, et al. ... Decreasing the fibronectin concentration by using small interfering RNA and inhibition by anti-fibronectin or anti-integrin ...
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 ... Integrin alpha6 D23.50.301.264.35.296 D23.50.301.264.35.355 D23.101.100.110.297 D23.101.100.110.355 Integrin alphaV 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 ... D23.101.100.110.288 D23.101.100.110.351 Integrin alpha2beta1 D12.776.543.750.70.200 D12.776.543.750.685.200 Integrin alpha3 ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
... by cross-linking MGAT5-modified complex N-glycans on alpha3beta1 integrin and subsequently activating alpha3beta1-integrin-Rac1 ... alpha3beta1 integrin was identified as the major Gal-3-binding protein in corneal epithelial cells by affinity chromatography ... Galectin-3 promotes lamellipodia formation in epithelial cells by interacting with complex N-glycans on alpha3beta1 integrin. ... revealed that carbohydrate-mediated interaction between Gal-3 and complex N-glycans on alpha3beta1 integrin plays a key role in ...
Integrin alpha2beta1 D12.776.543.750.72.200 D12.776.543.750.70.200 Integrin alpha3beta1 D12.776.543.750.72.300 Intellectual ... Integrin alpha1beta1 D12.776.543.750.72.100 D12.776.543.750.70.100 ...
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 ... Integrin alpha6 D23.50.301.264.35.296 D23.50.301.264.35.355 D23.101.100.110.297 D23.101.100.110.355 Integrin alphaV 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 ... D23.101.100.110.288 D23.101.100.110.351 Integrin alpha2beta1 D12.776.543.750.70.200 D12.776.543.750.685.200 Integrin alpha3 ...
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 ... Integrin alpha6 D23.50.301.264.35.296 D23.50.301.264.35.355 D23.101.100.110.297 D23.101.100.110.355 Integrin alphaV 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 ... D23.101.100.110.288 D23.101.100.110.351 Integrin alpha2beta1 D12.776.543.750.70.200 D12.776.543.750.685.200 Integrin alpha3 ...
... rojo cyclorana roja tragopan sungorus bacterium quadricarinatus hexachlorotellurate rohu alpha3beta4 alpha3beta2 alpha3beta1 ... reworded antithrombogenic hydroxyphenylacetamide ifng indirect clavisporus olfm4 vasospasm cebuella olfm1 azacitidine integrins ...
  • 1. Gangliosides inhibit urokinase-type plasminogen activator (uPA)-dependent squamous carcinoma cell migration by preventing uPA receptor/alphabeta integrin/epidermal growth factor receptor interactions. (nih.gov)
  • 3. Urokinase-type plasminogen activator binding to its receptor stimulates tumor cell migration by enhancing integrin-mediated signal transduction. (nih.gov)
  • 5. Critical role of integrin alpha 5 beta 1 in urokinase (uPA)/urokinase receptor (uPAR, CD87) signaling. (nih.gov)
  • 10. Interleukin-1alpha enhances the aggressive behavior of pancreatic cancer cells by regulating the alpha6beta1-integrin and urokinase plasminogen activator receptor expression. (nih.gov)
  • 11. Functional relevance of urinary-type plasminogen activator receptor-alpha3beta1 integrin association in proteinase regulatory pathways. (nih.gov)
  • 12. Urinary-type plasminogen activator (uPA) expression and uPA receptor localization are regulated by alpha 3beta 1 integrin in oral keratinocytes. (nih.gov)
  • 17. Convergence of the adhesive and fibrinolytic systems: recognition of urokinase by integrin alpha Mbeta 2 as well as by the urokinase receptor regulates cell adhesion and migration. (nih.gov)
  • 18. Activation of urokinase receptor by a novel interaction between the connecting peptide region of urokinase and alpha v beta 5 integrin. (nih.gov)
  • Mediates adhesion of proximal tubule epithelial cells via integrins alpha3-beta1 and alphaV-beta3. (nih.gov)
  • In 2003, we demonstrated that the mechanism of this anti-proliferative effect was independent of the metalloproteinase inhibitory activity by using the MMP-inhibitor null form Ala+TIMP-2, and was mediated by TIMP-2 binding to the alpha3 beta1 integrin on the surface of human microvascular endothelial cells. (nih.gov)
  • 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. (reference.md)
  • Integrins are heterodimeric integral membrane proteins composed of an alpha chain and a beta chain that function as cell surface adhesion molecules. (nih.gov)
  • Integrins are heterodimeric transmembrane receptors composed of non-covalently associated α and β subunits. (biomedcentral.com)
  • 14. Urokinase receptors promote beta1 integrin function through interactions with integrin alpha3beta1. (nih.gov)
  • Increasing evidence suggests that integrins are the most important receptors for cell metastasis [ 3 ]. (biomedcentral.com)
  • PI3K inhibitor LY294002 was used to explore the signal pathways of integrin α6 in HCC cells. (biomedcentral.com)
  • Knockdown integrin α6 can inhibit the proliferation and metastasis of HCC cells through PI3K/ARK and MAPK/ERK signal pathways by shRNA in vitro . (biomedcentral.com)
  • TIMP-2 cell surface binding and growth inhibitory activity is observed in both endothelial cells as well as tumor cells and results in a decrease in the association of protein tyrosine phosphate (PTP) activity with this integrin and an increase in PTP activity associated with variety of RTKs (VEGFR-2, FGFR1a, PDGFR and EGFR). (nih.gov)
  • 10 ] demonstrates that integrin α6β4 could regulate the migration and invasion of laminin (LN) to stimulate the metastasis potential of HCC. (biomedcentral.com)
  • 16. Myosin light chain kinase functions downstream of Ras/ERK to promote migration of urokinase-type plasminogen activator-stimulated cells in an integrin-selective manner. (nih.gov)
  • Two alternatively spliced isoforms of the alpha subunit (INTEGRIN ALPHA3), are differentially expressed in different cell types. (reference.md)
  • The gene encodes a member of the integrin alpha chain family of proteins. (nih.gov)
  • 6. Direct interaction of the kringle domain of urokinase-type plasminogen activator (uPA) and integrin alpha v beta 3 induces signal transduction and enhances plasminogen activation. (nih.gov)
  • This subunit joins with a beta 1 subunit to form an integrin that interacts with extracellular matrix proteins including members of the laminin family. (nih.gov)
  • At least 18 α and 8 β subunits have been identified so far, generating more than 24 members of the integrin family. (biomedcentral.com)
  • The integrins alpha3beta1 and alpha6beta1 physically and functionally associate with CD36 in human melanoma cells. (bvsalud.org)
  • Two human HCC cell lines, HepG2 and Bel-7402 were transfected with shRNA targeting human integrin α6. (biomedcentral.com)
  • In the current study, in order to explore the effect of integrin α6 in the process of HCC metastasis without the influence of β subunits and the molecular mechanisms involved, two human HCC cell line, HepG2 and Bel-7402 were transfected with short hairpin RNA (shRNA) targeting human integrin α6. (biomedcentral.com)
  • The aim of this study is to investigate the effect of short hairpin RNA (shRNA) silencing integrin α6 expression on the proliferation and metastasis in HCC cell lines. (biomedcentral.com)
  • Western blot and qRT-PCR detection showed that over 75% of integrin α6 expression in HCC cells was through knockdown by shRNA. (biomedcentral.com)
  • Furthermore, the metastatic mechanisms under high levels of expression of integrin α6 are still unclear. (biomedcentral.com)
  • 20. An all-D amino acid peptide model of alpha1(IV)531-543 from type IV collagen binds the alpha3beta1 integrin and mediates tumor cell adhesion, spreading, and motility. (nih.gov)
  • 7. Identification of CD47/integrin-associated protein and alpha(v)beta3 as two receptors for the alpha3(IV) chain of type IV collagen on tumor cells. (nih.gov)
  • Two alternatively spliced isoforms of the alpha subunit ( INTEGRIN ALPHA3 ), are differentially expressed in different cell types. (nih.gov)
  • In 2003, we demonstrated that the mechanism of this anti-proliferative effect was independent of the metalloproteinase inhibitory activity by using the MMP-inhibitor null form Ala+TIMP-2, and was mediated by TIMP-2 binding to the alpha3 beta1 integrin on the surface of human microvascular endothelial cells. (nih.gov)
  • Decreasing the fibronectin concentration by using small interfering RNA and inhibition by anti-fibronectin or anti-integrin antibodies blocked cleft formation and branching. (nih.gov)
  • 9. Colon cancer cells adhesion and spreading on autocrine laminin-10 is mediated by multiple integrin receptors and modulated by EGF receptor stimulation. (nih.gov)
  • 11. Mg2+ and Ca2+ differentially regulate beta 1 integrin-mediated adhesion of dermal fibroblasts and keratinocytes to various extracellular matrix proteins. (nih.gov)
  • Absence of alpha3beta1 leads to a reduction of Dab1, a signaling protein acting downstream of Reelin. (nih.gov)
  • The proteolytically remodeled laminin induced proliferation of dormant cancer cells by activating integrin α3β1 signaling. (nih.gov)
  • Thus, Reelin may arrest neuronal migration and promote normal cortical lamination by binding alpha3beta1 integrin and modulating integrin-mediated cellular adhesion. (nih.gov)
  • 2. Human skin mast cells express functional beta 1 integrins that mediate adhesion to extracellular matrix proteins. (nih.gov)
  • 6. Adhesion properties of human bladder cell lines with extracellular matrix components: the role of integrins and glycosylation. (nih.gov)
  • 8. Integrin alpha3beta1 engagement disrupts intercellular adhesion. (nih.gov)
  • 12. Different adhesion properties of highly and poorly metastatic HT-29 colon carcinoma cells with extracellular matrix components: role of integrin expression and cytoskeletal components. (nih.gov)
  • 19. The decreased adhesion of Y79 retinoblastoma cells to extracellular matrix proteins is due to a deficit of integrin receptors. (nih.gov)
  • TIMP-2 cell surface binding and growth inhibitory activity is observed in both endothelial cells as well as tumor cells and results in a decrease in the association of protein tyrosine phosphate (PTP) activity with this integrin and an increase in PTP activity associated with variety of RTKs (VEGFR-2, FGFR1a, PDGFR and EGFR). (nih.gov)