MMP-2 / CLG4A抗体

MMP-2 / CLG4A抗体

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  • 询价
  • Merck millipore
  • 中国/美国/德国
  • hz-10082-RP02
  • 2025年07月11日
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    • 详细信息
    • 技术资料
    • 保存条件

      常温,避光

    • 克隆性

      单克隆

    • 抗体名

      MMP-2 / CLG4A抗体

    MMP-2 / CLG4A抗体产品信息

    免疫原 :
    Recombinant human MMP-2 protein ( Catalog#10082-HNAH )
    Antibody Type : Rabbit Polyclonal Antibody ( Antibody Purification Platform )
    抗体宿主 :
    Rabbit IgG
    缓冲液 : 0.2 μm filtered solution in PBS, 5% trehalose may be added in some batches. Please read the hardcopy of COA or contact our customer service to confirm the formulation.
    制备方法 :
    Produced in rabbits immunized with purified, human cell-derived, recombinant human MMP2 ( rh MMP-2 ; Catalog#10082-HNAH ; NP_004521.1 ; Met 1 - Cys 660 ). MMP-2 specific IgG was purified by human MMP-2 affinity chromatography
    MMP-2 / CLG4A抗体背景综述
    Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that degrade components of the extracellular matrix (ECM) and play essential roles in various physiological processes such as morphogenesis, differentiation, angiogenesis and tissue remodeling, as well as pathological processes including inflammation, arthritis, cardiovascular diseases, pulmonary diseases and tumor invasion.
    72 kDa type I V collagenase, also known as Matrix metalloproteinase-2, Gelatinase A, MMP-2, and CLG4A, is a secreted protein which belongs to the peptidase M10A family. MMP-2 contains three fibronectin type-II domains and four hemopexin-like domains. MMP-2 is ubiquitinous metalloproteinase that is involved in diverse functions such as remodeling of the vasculature, angiogenesis, tissue repair, tumor invasion, inflammation, atherosclerotic plaque rupture, as well as degrading extracellular matrix proteins. MMP-2 can also act on several nonmatrix proteins such as big endothelial 1 and beta-type CGRP promoting vasoconstriction. MMP-2 cleaves KISS at a Gly-|-Leu bond and appears to have a role in myocardial cell death pathways. MMP-2 contributes to myocardial oxidative stress by regulating the activity of GSK3beta. Defects in MMP-2 are the cause of Torg-Winchester syndrome (TWS), also known as multicentric osteolysis nodulosis and arthropathy (MONA). TWS is an autosomal recessive osteolysis syndrome. It is severe with generalized osteolysis and osteopenia.
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