WNT1-inducible-signaling pathway protein 2

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WNT1 inducible signaling pathway protein 2
Identifiers
Symbols WISP2 ; CCN5; CT58; CTGF-L
External IDs OMIM603399 MGI1328326 HomoloGene2882 GeneCards: WISP2 Gene
RNA expression pattern
PBB GE WISP2 205792 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 8839 22403
Ensembl ENSG00000064205 ENSMUSG00000027656
UniProt O76076 Q9Z0G4
RefSeq (mRNA) NM_003881 NM_016873
RefSeq (protein) NP_003872 NP_058569
Location (UCSC) Chr 20:
43.34 – 43.36 Mb
Chr 2:
163.82 – 163.83 Mb
PubMed search [1] [2]

WNT1-inducible-signaling pathway protein 2, or WISP-2 (also named CCN5) is a matricellular protein that in humans is encoded by the WISP2 gene.[1][2]

Function[edit]

WISP-2 is a member of the CCN family (CCN intercellular signaling protein) of secreted, extracellular matrix (ECM)-associated signaling matricellular proteins. The CCN acronym is derived from the first three members of the family identified, namely CYR61 (CCN1), CTGF (connective tissue growth factor, or CCN2), and NOV. These proteins, together with WISP1/CCN4, WISP2 (CCN5, this gene), and WISP3 (CCN6) comprise the six-member CCN family in vertebrates. CCN proteins characteristically contain an N-terminal secretory signal peptide followed by four structurally distinct domains with homologies to insulin-like growth factor binding protein (IGFBP), von Willebrand type C repeats (vWC), thrombospondin type 1 repeat (TSR), and a cysteine knot motif within the C-terminal (CT) domain. However, WISP-2 is unique among this family of proteins by lacking precisely the CT domain (Figure). The CCN family of proteins regulates diverse cellular functions, including cell adhesion, migration, proliferation, differentiation.[3][4][5]

WISP-2 (CCN5) inhibits the proliferation of vascular smooth muscle cells,[6] human uterine myometrial cells, and leiomyoma cells.[7] Ectopic expression of WISP-2 also inhibits the motility and invasiveness of breast carcinoma cells.[8][9] WISP-2 also inhibits cardiac hypertrophy and fibrosis, an effect that appears linked to the absence of the CT domain.[10]

References[edit]

  1. ^ Jun JI, Lau LF (December 2011). "Taking aim at the extracellular matrix: CCN proteins as emerging therapeutic targets". Nat Rev Drug Discov 10 (12): 945–63. doi:10.1038/nrd3599. PMID 22129992. 
  2. ^ Russo JW, Castellot JJ (October 2010). "CCN5: biology and pathophysiology". J Cell Commun Signal 4 (3): 119–30. doi:10.1007/s12079-010-0098-7. PMC 2948116. PMID 21063502. 
  3. ^ Chen CC, Lau LF (April 2009). "Functions and mechanisms of action of CCN matricellular proteins". Int. J. Biochem. Cell Biol. 41 (4): 771–83. doi:10.1016/j.biocel.2008.07.025. PMC 2668982. PMID 18775791. 
  4. ^ Holbourn KP, Acharya KR, Perbal B (October 2008). "The CCN family of proteins: structure-function relationships". Trends Biochem. Sci. 33 (10): 461–73. doi:10.1016/j.tibs.2008.07.006. PMC 2683937. PMID 18789696. 
  5. ^ Leask A, Abraham DJ (December 2006). "All in the CCN family: essential matricellular signaling modulators emerge from the bunker". J. Cell. Sci. 119 (Pt 23): 4803–10. doi:10.1242/jcs.03270. PMID 17130294. 
  6. ^ Lake AC, Bialik A, Walsh K, Castellot JJ (January 2003). "CCN5 is a growth arrest-specific gene that regulates smooth muscle cell proliferation and motility". Am. J. Pathol. 162 (1): 219–31. doi:10.1016/S0002-9440(10)63813-8. PMC 1851113. PMID 12507905. 
  7. ^ Mason HR, Lake AC, Wubben JE, Nowak RA, Castellot JJ (March 2004). "The growth arrest-specific gene CCN5 is deficient in human leiomyomas and inhibits the proliferation and motility of cultured human uterine smooth muscle cells". Mol. Hum. Reprod. 10 (3): 181–7. doi:10.1093/molehr/gah028. PMID 14981145. 
  8. ^ Fritah A, Saucier C, De Wever O, et al. (February 2008). "Role of WISP-2/CCN5 in the maintenance of a differentiated and noninvasive phenotype in human breast cancer cells". Mol. Cell. Biol. 28 (3): 1114–23. doi:10.1128/MCB.01335-07. PMC 2223394. PMID 18070926. 
  9. ^ Banerjee S, Dhar G, Haque I, et al. (September 2008). "CCN5/WISP-2 expression in breast adenocarcinoma is associated with less frequent progression of the disease and suppresses the invasive phenotypes of tumor cells". Cancer Res. 68 (18): 7606–12. doi:10.1158/0008-5472.CAN-08-1461. PMID 18794149. 
  10. ^ Yoon PO, Lee MA, Cha H, et al. (August 2010). "The opposing effects of CCN2 and CCN5 on the development of cardiac hypertrophy and fibrosis". J. Mol. Cell. Cardiol. 49 (2): 294–303. doi:10.1016/j.yjmcc.2010.04.010. PMID 20430035.