Vitronectin/S-Protein Antibody [G14H11]

Application: Reactivity: Human

Lane 1: Human serum

Usage Information

Dilution
WB1:2000 - 1:10000 IHC1:100 IF1:50 - 1:100

Application
WB, IHC, IF

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
54 kDa 75 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human serum tissue; Human liver tissue; HepG2 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
Vitronectin/S-Protein Antibody [G14H11] detects endogenous levels of total Vitronectin/S protein.

Clone
G14H11

Synonym(s)
Vitronectin, VN, S-protein, Serum-spreading factor, V75, VTN

Background
Vitronectin (VTN/S-Protein), a conformationally dynamic 478-amino-acid glycoprotein (~75 kDa) secreted by hepatocytes into plasma and incorporated into ECM as single-chain or proteolytically cleaved two-chain (65/10 kDa) multimers linked by Cys156–Cys472 disulfide, orchestrates cell-ECM adhesion, coagulation-fibrinolysis balance, and complement regulation through ligand-inducible structural transitions. The N-terminal somatomedin B domain (residues 1–44, cysteine-knot with four intradomain disulfides) binds PAI-1/uPAR to stabilize antiprotease activity, while the cryptic RGD motif (Arg45-Gly46-Asp47) in the flexible hinge exposes upon "open" conformation for high-affinity αvβ3/αvβ5/αIIbβ3 integrin ligation, triggering FAK/Src-PI3K/AKT-YAP/TAZ mechanosignaling for migration/proliferation; three polybasic heparin-binding domains (HBD1–3) anchor glycosaminoglycans, and C-terminal hemopexin-like β-propeller (four HX repeats, residues 128–478) serves as multivalent hub docking collagen IV/X/tenascin/plasminogen via HX2–3 interfaces. Vitronectin restrains terminal complement by binding C5b-7 to block MAC pore formation, protects endothelium during thrombosis via thrombin-antithrombin trapping, and coordinates wound healing through RGD-integrin-ECM haptotaxis. It drives cancer metastasis (breast/ovarian) via MMP2/9 activation and uPAR signaling, accumulates in atherosclerotic plaques/fibrotic stroma enhancing collagen stability, facilitates bacterial pathogenesis (Yersinia Ail-mediated complement evasion), and deposits in AMD drusen/AD amyloid plaques, positioning RGD-mimetic antagonists and HX-domain inhibitors as therapeutics for thrombosis, tumor invasion, and sterile inflammation.

Background

Vitronectin (VTN/S-Protein), a conformationally dynamic 478-amino-acid glycoprotein (~75 kDa) secreted by hepatocytes into plasma and incorporated into ECM as single-chain or proteolytically cleaved two-chain (65/10 kDa) multimers linked by Cys156–Cys472 disulfide, orchestrates cell-ECM adhesion, coagulation-fibrinolysis balance, and complement regulation through ligand-inducible structural transitions. The N-terminal somatomedin B domain (residues 1–44, cysteine-knot with four intradomain disulfides) binds PAI-1/uPAR to stabilize antiprotease activity, while the cryptic RGD motif (Arg45-Gly46-Asp47) in the flexible hinge exposes upon "open" conformation for high-affinity αvβ3/αvβ5/αIIbβ3 integrin ligation, triggering FAK/Src-PI3K/AKT-YAP/TAZ mechanosignaling for migration/proliferation; three polybasic heparin-binding domains (HBD1–3) anchor glycosaminoglycans, and C-terminal hemopexin-like β-propeller (four HX repeats, residues 128–478) serves as multivalent hub docking collagen IV/X/tenascin/plasminogen via HX2–3 interfaces. Vitronectin restrains terminal complement by binding C5b-7 to block MAC pore formation, protects endothelium during thrombosis via thrombin-antithrombin trapping, and coordinates wound healing through RGD-integrin-ECM haptotaxis. It drives cancer metastasis (breast/ovarian) via MMP2/9 activation and uPAR signaling, accumulates in atherosclerotic plaques/fibrotic stroma enhancing collagen stability, facilitates bacterial pathogenesis (Yersinia Ail-mediated complement evasion), and deposits in AMD drusen/AD amyloid plaques, positioning RGD-mimetic antagonists and HX-domain inhibitors as therapeutics for thrombosis, tumor invasion, and sterile inflammation.

References
https://pubmed.ncbi.nlm.nih.gov/31535027/ https://pubmed.ncbi.nlm.nih.gov/20807208/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%