CTGF

Connective tissue growth factor
Identifiers
Symbol(s)	CTGF; CCN2; HCS24; IGFBP8; MGC102839; NOV2
External IDs	OMIM: 121009 MGI: 95537 Homologene: 1431
Gene Ontology Molecular Function: • integrin binding • protein binding • insulin-like growth factor binding • heparin binding Cellular Component: • extracellular region • proteinaceous extracellular matrix • extracellular space • soluble fraction • plasma membrane Biological Process: • cartilage condensation • ossification • angiogenesis • regulation of cell growth • DNA replication • cell adhesion • cell-matrix adhesion • integrin-mediated signaling pathway • fibroblast growth factor receptor signaling pathway • epidermis development • response to wounding • cell migration • cell differentiation
RNA expression pattern
Additional recommended knowledge Daily Visual Balance Check Safe Weighing Range Ensures Accurate Results What is the Sensitivity of my Balance? More reference expression data
Orthologs
	Human	Mouse
Entrez	1490	14219
Ensembl	ENSG00000118523	ENSMUSG00000019997
Uniprot	P29279	Q91V29
Refseq	NM_001901 (mRNA) NP_001892 (protein)	NM_010217 (mRNA) NP_034347 (protein)
Location	Chr 6: 132.31 - 132.31 Mb	Chr 10: 24.28 - 24.29 Mb
Pubmed search	[1]	[2]

CTGF (connective tissue growth factor) is a cysteine-rich, matrix-associated, heparin-binding protein. In vitro, CTGF mirrors some of the effects of TGF beta on skin fibroblasts, such as stimulation of extracellular matrix production, chemotaxis, proliferation and integrin expression. CTGF can promote endothelial cell growth, migration, adhesion and survival and is thus implicated in endothelial cell function and angiogenesis^[1].

CTGF binds to perlecan^[2], a proteoglycan which has been localised in synovium, cartilage and numerous other tissues.

CTGF has been implicated in extracellular matrix remodelling in wound healing, scleroderma and other fibrotic processes, as it is capable of upregulating both matrix metalloproteinases (MMPs) and their inhibitors (TIMPs). Therefore, CTGF has the potential to activate both the synthesis and degradation of the extracellular matrix.

Knockout mice which have had the gene for CTGF removed do not develop normally. Impaired chondrocyte proliferation, angiogenesis, extracellular matrix production and turnover leads to abnormal skeletal growth.^[3]

References

Further reading