CTGF Antibody [P10H5] | Primary Antibodies

Application: Reactivity: Mouse, Human, Rat

Usage Information

Dilution
WB1:1000 IP1:30 IF1:100

Application
WB, IP, IF

Reactivity
Mouse, Human, Rat

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
37 kDa 37 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
CTGF Antibody [P10H5] detects endogenous levels of total CTGF protein.

Clone
P10H5

Synonym(s)
CTGF, HCS24, IGFBP8, CCN2, CCN family member 2, Cellular communication network factor 2, Connective tissue growth factor, Hypertrophic chondrocyte-specific protein 24, Insulin-like growth factor-binding protein 8, IBP-8, IGF-binding protein 8, IGFBP-8

Background
CTGF, or connective tissue growth factor, belongs to the CCN family of matricellular proteins characterized by modular domains that enable diverse interactions in the extracellular matrix. It features an insulin-like growth factor-binding protein domain, von Willebrand factor type C repeat, thrombospondin type 1 repeat, and cysteine-rich C-terminal domain, which collectively facilitate binding to integrins, LRP receptors, HSPGs, VEGF, TGF-β superfamily members, fibronectin, and BMPs. Secreted into the matrix, CTGF binds cell surface integrins like αvβ3, α5β1, and α6β1 to activate FAK/Src/ERK, PI3K/Akt, and NF-κB pathways, promoting fibroblast adhesion, migration, myofibroblast transdifferentiation, and extracellular matrix deposition including collagen I and fibronectin. Through TSP1 domain interaction with VEGF, it modulates angiogenesis by sequestering VEGF or releasing it via RhoA inactivation, while VWC domain antagonizes BMP-2/7 signaling and chaperones TGF-β to enhance SMAD2/3-mediated transcription. YAP/TAZ from the Hippo pathway transactivate CTGF expression via TEAD binding, forming feedback loops that drive sustained matrix remodeling, and CTGF reciprocates by stabilizing YAP nuclear localization. CTGF supports skeletal development by regulating chondrocyte proliferation and osteoblast differentiation, wound repair through myofibroblast activation, and vascular integrity via barrier formation. TGF-β, angiotensin II, hypoxia, and mechanical stress induce CTGF via SMAD, MAPK, and ETS1 promoters, amplifying profibrotic responses in liver, lung, kidney, and heart fibrosis where it cooperates with TGF-β for persistent collagen accumulation. Elevated in desmoplastic tumors like pancreatic cancer, CTGF fosters EMT via integrin-linked kinase/ERK/PI3K, tumor stroma deposition, and metastasis, though context-dependent suppression occurs in some lung and colorectal cancers.

Background

CTGF, or connective tissue growth factor, belongs to the CCN family of matricellular proteins characterized by modular domains that enable diverse interactions in the extracellular matrix. It features an insulin-like growth factor-binding protein domain, von Willebrand factor type C repeat, thrombospondin type 1 repeat, and cysteine-rich C-terminal domain, which collectively facilitate binding to integrins, LRP receptors, HSPGs, VEGF, TGF-β superfamily members, fibronectin, and BMPs. Secreted into the matrix, CTGF binds cell surface integrins like αvβ3, α5β1, and α6β1 to activate FAK/Src/ERK, PI3K/Akt, and NF-κB pathways, promoting fibroblast adhesion, migration, myofibroblast transdifferentiation, and extracellular matrix deposition including collagen I and fibronectin. Through TSP1 domain interaction with VEGF, it modulates angiogenesis by sequestering VEGF or releasing it via RhoA inactivation, while VWC domain antagonizes BMP-2/7 signaling and chaperones TGF-β to enhance SMAD2/3-mediated transcription. YAP/TAZ from the Hippo pathway transactivate CTGF expression via TEAD binding, forming feedback loops that drive sustained matrix remodeling, and CTGF reciprocates by stabilizing YAP nuclear localization. CTGF supports skeletal development by regulating chondrocyte proliferation and osteoblast differentiation, wound repair through myofibroblast activation, and vascular integrity via barrier formation. TGF-β, angiotensin II, hypoxia, and mechanical stress induce CTGF via SMAD, MAPK, and ETS1 promoters, amplifying profibrotic responses in liver, lung, kidney, and heart fibrosis where it cooperates with TGF-β for persistent collagen accumulation. Elevated in desmoplastic tumors like pancreatic cancer, CTGF fosters EMT via integrin-linked kinase/ERK/PI3K, tumor stroma deposition, and metastasis, though context-dependent suppression occurs in some lung and colorectal cancers.

References
https://pubmed.ncbi.nlm.nih.gov/23259531/ https://pubmed.ncbi.nlm.nih.gov/35847511/

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%