CYR61 Antibody [M15N8] | Primary Antibodies

Application: Reactivity: Human, Mouse

Lane 1: OVCAR8, Lane 2: Hela, Lane 3: Saso-2, Lane 4: C2C12

Usage Information

Dilution
WB1:1000 IHC1:50

Application
WB, IHC

Reactivity
Human, Mouse

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
41 kDa

Positive Control	Human urothelial carcinoma; Human lung adenocarcinoma; Human pancreatic neuroendocrine tumor; Human prostate adenocarcinoma; OVCAR8 cells; HeLa cells; Saos-2 cells; C2C12 cells
Negative Control	MCF7 cells; HT-29 cells

Datasheet & SDS

Biological Description

Specificity
CYR61 Antibody [M15N8] detects endogenous levels of total CYR61 protein.

Clone
M15N8

Synonym(s)
CCN1; CCN family member 1; Cellular communication network factor 1; Cysteine-rich angiogenic inducer 61; Insulin-like growth factor-binding protein 10 (IBP-10; IGF-binding protein 10; IGFBP-10); Protein CYR61; Protein GIG1; CYR61; GIG1; IGFBP10

Background
Cysteine-rich protein 61 (CYR61, also known as CCN1) is a secreted matricellular protein of the CCN family distinguished by its high cysteine content forming disulfide bonds that stabilize its structure, featuring four conserved modular domains from N- to C-terminus: an insulin-like growth factor-binding protein (IGFBP)-like domain (Module I) with 68 amino acids for low-affinity IGF interactions, a von Willebrand factor type C repeat (vWC) domain (Module II) involved in dimerization and heparin binding, a thrombospondin type 1 repeat (TSP-1) domain (Module III) critical for integrin αvβ3 and α6β1 engagement, and a C-terminal cysteine-knot domain (Module IV) mediating receptor binding and multimerization on the extracellular matrix. CYR61 orchestrates diverse context-dependent cellular responses by binding distinct integrins and heparan sulfate proteoglycans (HSPGs) like syndecan-4, promoting angiogenesis through αvβ3-mediated endothelial proliferation, VEGF upregulation, and recruitment of CD34+ progenitors while inducing apoptosis via α6β1/HSPG complexes that trigger ROS production via RAC-1, 5-lipoxygenase, NADPH oxidase, and mitochondria, leading to sustained JNK activation, c-FLIP degradation, caspase-8/10 signaling, and p53-mediated DNA damage responses in fibroblasts and endothelial cells. It drives cardiovascular and skeletal development including placental vessel bifurcation, hypertrophic cartilage neovascularization, osteoblast differentiation via αvβ3/ILK, and osteoclast inhibition, whereas in tumorigenesis its overexpression correlates with progression in breast, lung, and hepatocellular carcinoma via Wnt/β-catenin or hypoxia-inducible factor-1α regulation, yet inversely with prostate cancer aggressiveness.

Background

Cysteine-rich protein 61 (CYR61, also known as CCN1) is a secreted matricellular protein of the CCN family distinguished by its high cysteine content forming disulfide bonds that stabilize its structure, featuring four conserved modular domains from N- to C-terminus: an insulin-like growth factor-binding protein (IGFBP)-like domain (Module I) with 68 amino acids for low-affinity IGF interactions, a von Willebrand factor type C repeat (vWC) domain (Module II) involved in dimerization and heparin binding, a thrombospondin type 1 repeat (TSP-1) domain (Module III) critical for integrin αvβ3 and α6β1 engagement, and a C-terminal cysteine-knot domain (Module IV) mediating receptor binding and multimerization on the extracellular matrix. CYR61 orchestrates diverse context-dependent cellular responses by binding distinct integrins and heparan sulfate proteoglycans (HSPGs) like syndecan-4, promoting angiogenesis through αvβ3-mediated endothelial proliferation, VEGF upregulation, and recruitment of CD34+ progenitors while inducing apoptosis via α6β1/HSPG complexes that trigger ROS production via RAC-1, 5-lipoxygenase, NADPH oxidase, and mitochondria, leading to sustained JNK activation, c-FLIP degradation, caspase-8/10 signaling, and p53-mediated DNA damage responses in fibroblasts and endothelial cells. It drives cardiovascular and skeletal development including placental vessel bifurcation, hypertrophic cartilage neovascularization, osteoblast differentiation via αvβ3/ILK, and osteoclast inhibition, whereas in tumorigenesis its overexpression correlates with progression in breast, lung, and hepatocellular carcinoma via Wnt/β-catenin or hypoxia-inducible factor-1α regulation, yet inversely with prostate cancer aggressiveness.

References
https://pubmed.ncbi.nlm.nih.gov/29115499/ https://pubmed.ncbi.nlm.nih.gov/21805345/

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%