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Integrin αVβ3 Antibody [C22M19]

Cat.No.: F2133

Application: Reactivity: Rat, Chicken, Human

Usage Information

Dilution

Application
IP, IHC, IF, FCM

Reactivity
Rat, Chicken, Human

Source
Mouse 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

Datasheet & SDS

Biological Description

Specificity
Integrin αVβ3 Antibody [C22M19] detects endogenous levels of total Integrin αVβ3 protein.

Clone
C22M19

Synonym(s)
CD51; MSK8; VNRA; VTNR; ITGAV; Integrin alpha-V; Vitronectin receptor; Vitronectin receptor subunit alpha

Background
Integrin αVβ3, a promiscuous RGD-binding heterodimeric adhesion receptor ubiquitously expressed on endothelial cells, platelets, osteoclasts, and tumor cells, assembles a headpiece with αV's seven-bladed β-propeller and thigh domains atop β3's βI (vWFA-like with metal ion-dependent adhesion site, MIDAS), hybrid, and PSI domains, extended via calf-1/2 (αV) and EGF-like IE1-4 plus β-tail (β3) legs bent at genuflexed knees in the low-affinity closed conformation, with short transmembrane helices and cytoplasmic tails enabling talin-mediated inside-out activation. Ligand engagement at the αV propeller-βI interface (coordinated by Mn²⁺/Mg²⁺/Ca²⁺ at MIDAS, ADMIDAS, and LIMBS) triggers headpiece opening (~130° swing), knee extension, and rigid-body separation of α/β TM helices, propagating "switchblade-like" conformational waves that cluster receptors into high-avidity states for firm adhesion while recruiting FAK/Src/paxillin to activate PI3K/Akt, MAPK/ERK, and Rho GTPase pathways driving angiogenesis, migration, survival, and matrix remodeling; conversely, outside-in signaling via force-dependent catch bonds (~10-fold affinity increase under shear) reinforces cytoskeletal anchorage. Dysregulated αVβ3 promotes pathological neovascularization in tumors/age-related macular degeneration, osteoclast-mediated bone resorption in osteoporosis, thrombosis via platelet aggregation on vitronectin/fibronectin, and arterial remodeling in atherosclerosis, while therapeutic antagonists or mutations disrupting the IE2-thigh interface impair activation and suppress these processes.

Background

Integrin αVβ3, a promiscuous RGD-binding heterodimeric adhesion receptor ubiquitously expressed on endothelial cells, platelets, osteoclasts, and tumor cells, assembles a headpiece with αV's seven-bladed β-propeller and thigh domains atop β3's βI (vWFA-like with metal ion-dependent adhesion site, MIDAS), hybrid, and PSI domains, extended via calf-1/2 (αV) and EGF-like IE1-4 plus β-tail (β3) legs bent at genuflexed knees in the low-affinity closed conformation, with short transmembrane helices and cytoplasmic tails enabling talin-mediated inside-out activation. Ligand engagement at the αV propeller-βI interface (coordinated by Mn²⁺/Mg²⁺/Ca²⁺ at MIDAS, ADMIDAS, and LIMBS) triggers headpiece opening (~130° swing), knee extension, and rigid-body separation of α/β TM helices, propagating "switchblade-like" conformational waves that cluster receptors into high-avidity states for firm adhesion while recruiting FAK/Src/paxillin to activate PI3K/Akt, MAPK/ERK, and Rho GTPase pathways driving angiogenesis, migration, survival, and matrix remodeling; conversely, outside-in signaling via force-dependent catch bonds (~10-fold affinity increase under shear) reinforces cytoskeletal anchorage. Dysregulated αVβ3 promotes pathological neovascularization in tumors/age-related macular degeneration, osteoclast-mediated bone resorption in osteoporosis, thrombosis via platelet aggregation on vitronectin/fibronectin, and arterial remodeling in atherosclerosis, while therapeutic antagonists or mutations disrupting the IE2-thigh interface impair activation and suppress these processes.

References
https://pubmed.ncbi.nlm.nih.gov/23106217/ https://pubmed.ncbi.nlm.nih.gov/19704023/

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%