CCN family member 3 (P48745)

Uniprot ID	P48745
Protein Name	CCN family member 3
Gene Name	CCN3
Species	Homo sapiens (Human)

Signal peptide^(a)	Y	Secretome P^(b)	0.898
Function	Immediate-early protein playing a role in various cellular processes including proliferation, adhesion, migration, differentiation and survival (PubMed:15181016, PubMed:15611078, PubMed:12695522, PubMed:21344378, PubMed:12050162). Acts by binding to integrins or membrane receptors such as NOTCH1 (PubMed:12695522, PubMed:21344378, PubMed:15611078). Essential regulator of hematopoietic stem and progenitor cell function (PubMed:17463287). Inhibits myogenic differentiation through the activation of Notch-signaling pathway (PubMed:12050162). Inhibits vascular smooth muscle cells proliferation by increasing expression of cell-cycle regulators such as CDKN2B or CDKN1A independently of TGFB1 signaling (PubMed:20139355). Ligand of integrins ITGAV:ITGB3 and ITGA5:ITGB1, acts directly upon endothelial cells to stimulate pro-angiogenic activities and induces angiogenesis. In endothelial cells, supports cell adhesion, induces directed cell migration (chemotaxis) and promotes cell survival (PubMed:12695522). Plays also a role in cutaneous wound healing acting as integrin receptor ligand. Supports skin fibroblast adhesion through ITGA5:ITGB1 and ITGA6:ITGB1 and induces fibroblast chemotaxis through ITGAV:ITGB5. Seems to enhance bFGF-induced DNA synthesis in fibroblasts (PubMed:15611078). Involved in bone regeneration as a negative regulator (By similarity). Enhances the articular chondrocytic phenotype, whereas it repressed the one representing endochondral ossification (PubMed:21871891). Impairs pancreatic beta-cell function, inhibits beta-cell proliferation and insulin secretion (By similarity). Plays a role as negative regulator of endothelial pro-inflammatory activation reducing monocyte adhesion, its anti-inflammatory effects occur secondary to the inhibition of NF-kappaB signaling pathway (PubMed:21063504). Contributes to the control and coordination of inflammatory processes in atherosclerosis (By similarity). Attenuates inflammatory pain through regulation of IL1B-and TNF-induced MMP9, MMP2 and CCL2 expression. Inhibits MMP9 expression through ITGB1 engagement (PubMed:21871891). .
GO - Molecular function	growth factor activity : IEA:UniProtKB-KW heparin binding : IBA:GO_Central insulin-like growth factor binding : IEA:InterPro integrin binding : IPI:UniProtKB Notch binding : IPI:UniProtKB
GO - Biological process	angiogenesis : IDA:UniProtKB bone regeneration : ISS:UniProtKB cell adhesion : IBA:GO_Central cell adhesion mediated by integrin : IDA:UniProtKB cell chemotaxis : IDA:UniProtKB chondrocyte differentiation : IMP:UniProtKB endothelial cell chemotaxis : IDA:UniProtKB endothelial cell-cell adhesion : IDA:UniProtKB fibroblast migration : IDA:UniProtKB hematopoietic stem cell homeostasis : IMP:UniProtKB negative regulation of cell death : IBA:GO_Central negative regulation of cell growth : IMP:UniProtKB negative regulation of chondrocyte proliferation : IMP:UniProtKB negative regulation of inflammatory response : ISS:UniProtKB negative regulation of insulin secretion : ISS:UniProtKB negative regulation of monocyte chemotaxis : IMP:UniProtKB negative regulation of myotube differentiation : IDA:UniProtKB negative regulation of NIK/NF-kappaB signaling : IMP:UniProtKB negative regulation of sensory perception of pain : ISS:UniProtKB negative regulation of SMAD protein signal transduction : ISS:UniProtKB positive regulation of Notch signaling pathway : IDA:UniProtKB regulation of gene expression : IEA:Ensembl smooth muscle cell migration : IDA:UniProtKB smooth muscle cell proliferation : IDA:UniProtKB type B pancreatic cell proliferation : ISS:UniProtKB

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^{(a) The Signal peptide D-score cutoff for "YES"(having signal peptide) is 0.45.}
^{(b) Non-classically secreted proteins should obtain an NN-score(Neural Networks score) exceeding the normal threshold of 0.5, but not at the same time be predicted to contain a signal peptide.}