Regulator of cell cycle RGCC

RGCC
Identifiers
AliasesRGCC, C13orf15, RGC-32, RGC32, bA157L14.2, regulator of cell cycle
External IDsMGI: 1913464 HomoloGene: 8544 GeneCards: RGCC
Gene location (Human)
Chr.Chromosome 13 (human)[1]
Band13q14.11Start41,457,559 bp[1]
End41,470,882 bp[1]
RNA expression pattern
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez

28984

66214

Ensembl

ENSG00000102760

ENSMUSG00000022018

UniProt

Q9H4X1

Q9DBX1

RefSeq (mRNA)

NM_014059

NM_025427

RefSeq (protein)

NP_054778

NP_079703

Location (UCSC)Chr 13: 41.46 – 41.47 MbChr 14: 79.29 – 79.3 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Regulator of cell cycle RGCC (RGCC) also known as response gene to complement 32 protein (RGC-32) is a protein that in humans is encoded by the RGCC gene.[5][6][7]

Function

This gene is thought to regulate cell cycle progression. It is induced by p53 in response to DNA damage, or by sublytic levels of complement system proteins that result in activation of the cell cycle. The encoded protein localizes to the cytoplasm during interphase and to centrosomes during mitosis. The protein forms a complex with polo-like kinase 1. The protein also translocates to the nucleus in response to treatment with complement system proteins, and can associate with and increase the kinase activity of cell division cycle 2 protein. In different assays and cell types, overexpression of this protein has been shown to activate or suppress cell cycle progression.[7]

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000102760 - Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000022018 - Ensembl, May 2017
  3. "Human PubMed Reference:".
  4. "Mouse PubMed Reference:".
  5. Saigusa K, Imoto I, Tanikawa C, Aoyagi M, Ohno K, Nakamura Y, Inazawa J (Feb 2007). "RGC32, a novel p53-inducible gene, is located on centrosomes during mitosis and results in G2/M arrest". Oncogene. 26 (8): 1110–21. doi:10.1038/sj.onc.1210148. PMID 17146433.
  6. Huang WY, Li ZG, Rus H, Wang X, Jose PA, Chen SY (Mar 2009). "RGC-32 mediates transforming growth factor-beta-induced epithelial-mesenchymal transition in human renal proximal tubular cells". J Biol Chem. 284 (14): 9426–32. doi:10.1074/jbc.M900039200. PMC 2666595. PMID 19158077.
  7. 1 2 "Entrez Gene: RGC32 response gene to complement 32".

Further reading

  • Fosbrink M, Niculescu F, Rus H (2005). "The role of c5b-9 terminal complement complex in activation of the cell cycle and transcription". Immunol. Res. 31 (1): 37–46. doi:10.1385/IR:31:1:37. PMID 15591621.
  • Bonaldo MF, Lennon G, Soares MB (1997). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Res. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548.
  • Badea TC, Niculescu FI, Soane L, et al. (1998). "Molecular cloning and characterization of RGC-32, a novel gene induced by complement activation in oligodendrocytes". J. Biol. Chem. 273 (41): 26977–81. doi:10.1074/jbc.273.41.26977. PMID 9756947.
  • Badea T, Niculescu F, Soane L, et al. (2002). "RGC-32 increases p34CDC2 kinase activity and entry of aortic smooth muscle cells into S-phase". J. Biol. Chem. 277 (1): 502–8. doi:10.1074/jbc.M109354200. PMID 11687586.
  • Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
  • Fosbrink M, Cudrici C, Niculescu F, et al. (2005). "Overexpression of RGC-32 in colon cancer and other tumors". Exp. Mol. Pathol. 78 (2): 116–22. doi:10.1016/j.yexmp.2004.11.001. PMID 15713436.
  • Tanaka T, Takada H, Nomura A, et al. (2005). "Distinct gene expression patterns of peripheral blood cells in hyper-IgE syndrome". Clin. Exp. Immunol. 140 (3): 524–31. doi:10.1111/j.1365-2249.2005.02805.x. PMC 1809394. PMID 15932515.
  • Olsen JV, Blagoev B, Gnad F, et al. (2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635–48. doi:10.1016/j.cell.2006.09.026. PMID 17081983.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.