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Rabbit Anti-Collagen VIII alpha 1/BF488 Conjugated antibody (bs-7529R-BF488)
訂購熱線:400-901-9800
訂購郵箱:sales@bioss.com.cn
訂購QQ:  400-901-9800
技術支持:techsupport@bioss.com.cn
說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-7529R-BF488
英文名稱 Rabbit Anti-Collagen VIII alpha 1/BF488 Conjugated antibody
中文名稱 BF488標記的8型膠原/內皮膠原蛋白抗體
別    名 C3orf7; CO8A1_HUMAN; COL8A1; Collagen alpha 1(VIII) chain [Precursor]; Endothelial collagen; MGC9568; Vastatin.  
規格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 心血管  信號轉導  糖尿病  細胞骨架  細胞外基質  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 Mouse, Rat,  (predicted: Human, Chicken, Dog, Pig, Cow, )
產品應用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 19/79kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human Collagen VIII alpha 1 (672-718aa)
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產品介紹 background:
Macromolecular component of the subendothelium. Major component of the Descemet's membrane (basement membrane) of corneal endothelial cells. Also component of the endothelia of blood vessels. Necessary for migration and proliferation of vascular smooth muscle cells and thus, has a potential role in the maintenance of vessel wall integrity and structure, in particular in artherogenesis. Vastatin, the C-terminal fragment comprising the NC1 domain, inhibits aortic endothelial cell proliferation and causes cell apoptosis.


Function:
Macromolecular component of the subendothelium. Major component of the Descemet's membrane (basement membrane) of corneal endothelial cells. Also component of the endothelia of blood vessels. Necessary for migration and proliferation of vascular smooth muscle cells and thus, has a potential role in the maintenance of vessel wall integrity and structure, in particular in atherogenesis.
Vastatin, the C-terminal fragment comprising the NC1 domain, inhibits aortic endothelial cell proliferation and causes cell apoptosis.

Subunit:
Homodimer; antiparallel disulfide-linked dimer. Heterodimer with PDGFB; antiparallel disulfide-linked dimer. The PDGFA homodimer interacts with PDGFRA homodimers, and with heterodimers formed by PDGFRA and PDGFRB. The heterodimer composed of PDGFA and PDGFB interacts with PDGFRA homodimers, and with heterodimers formed by PDGFRA and PDGFRB. Interacts with CSPG4.

Subcellular Location:
Secreted, extracellular space, extracellular matrix, basement membrane.

Tissue Specificity:
Expressed primarily in the subendothelium of large blood vessels. Also expressed in arterioles and venules in muscle, heart, kidney, spleen, umbilical cord, liver and lung and is also found in connective tissue layers around hair follicles, around nerve bundles in muscle, in the dura of the optic nerve, in cornea and sclera, and in the perichondrium of cartilaginous tissues. In the kidney, expressed in mesangial cells, glomerular endothelial cells, and tubular epithelial cells. Also expressed in mast cells, and in astrocytes during the repair process. Expressed in Descemet's membrane. Specifically expressed in peritoneal fibroblasts and mesothelial cells.

Post-translational modifications:
Prolines at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains.
Proteolytically cleaved by neutrophil elastase, in vitro. Proteolytic processing produces the C-terminal NC1 domain fragment, vastatin.

Similarity:
Belongs to the PDGF/VEGF growth factor family.

Database links:
UniProtKB/Swiss-Prot: P27658.2

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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