Collagen IV alpha 1 Monoclonal / Unconjugated / MC4-HA

Product Details
Description This monoclonal antibody reacts with native human collagen type IV, and with heat- denatured collagen IV form in ELISA and immunoblots. There is no cross-reactivity with human collagen I, II, III and V. It stains exclusively basement membranes on cryostat sections of human tissues such as kidney, liver and heart. The extent of expression of the basement membrane component type IV collagen may be correlated with the degree of differentiation of basement membrane producing neoplasms. Neoplastic cells of invasive carcinomas often lack a continuous basement membrane. In diagnostic histopathology antibodies to type IV collagen may help to distinguish between non-invasive (benign or in situ) and invasive lesions. Furthermore the antibody is important in the differential diagnosis of bullous lesions in dermatopathology. In in vitro studies with endothelial cells and smooth muscle cells the antibody is helpful in detection of production collagen type IV. This antibody reacts also with dog collagen IV on cryostate and paraffin sections.
Conjugate Unconjugated
Clone MC4-HA
Target Species Human
Applications ELISA, IHC-P, IHC-Fr, IHC
Supplier Novus Biologicals
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About Collagen IV alpha 1
This gene encodes a type IV collagen alpha protein. Type IV collagen proteins are integral components of basement membranes. This gene shares a bidirectional promoter with a paralogous gene on the opposite strand. The protein consists of an amino-terminal 7S domain, a triple-helix forming collagenous domain, and a carboxy-terminal non-collagenous domain. It functions as part of a heterotrimer and interacts with other extracellular matrix components such as perlecans, proteoglycans, and laminins. In addition, proteolytic cleavage of the non-collagenous carboxy-terminal domain results in a biologically active fragment known as arresten, which has anti-angiogenic and tumor suppressor properties. Mutations in this gene cause porencephaly, cerebrovascular disease, and renal and muscular defects. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Dec 2014]
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