HIC1

Hypermethylated in cancer 1
Identifiers
Symbols	HIC1; ZBTB29; ZNF901; hic-1
External IDs	OMIM: 603825 MGI: 1338010 HomoloGene: 4740 GeneCards: HIC1 Gene
Gene Ontology Molecular function • DNA binding • sequence-specific DNA binding transcription factor activity • protein binding • zinc ion binding • histone deacetylase binding • sequence-specific DNA binding • metal ion binding Cellular component • chromatin • nucleus • nucleolus • cytoplasm Biological process • negative regulation of transcription from RNA polymerase II promoter • transcription, DNA-dependent • regulation of transcription, DNA-dependent • multicellular organismal development • intrinsic apoptotic signaling pathway in response to DNA damage • Wnt receptor signaling pathway • negative regulation of Wnt receptor signaling pathway • positive regulation of DNA damage response, signal transduction by p53 class mediator Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	3090	15248
Ensembl	ENSG00000177374	ENSMUSG00000043099
UniProt	Q14526	Q9R1Y5
RefSeq (mRNA)	NM_001098202	NM_001098203
RefSeq (protein)	NP_001091672	NP_001091673
Location (UCSC)	Chr 17: 1.96 – 1.96 Mb	Chr 11: 75.16 – 75.17 Mb
PubMed search	[1]	[2]

Hypermethylated in cancer 1 protein is a protein that in humans is encoded by the HIC1 gene.

Further reading

• Chopin V, Leprince D (2006). "[Chromosome arm 17p13.3: could HIC1 be the one ?]". Med Sci (Paris) 22 (1): 54–61. doi:10.1051/medsci/200622154. PMID 16386221. 
• Wales MM, Biel MA, el Deiry W, et al. (1995). "p53 activates expression of HIC-1, a new candidate tumour suppressor gene on 17p13.3.". Nat. Med. 1 (6): 570–7. doi:10.1038/nm0695-570. PMID 7585125. 
• Fujii H, Biel MA, Zhou W, et al. (1998). "Methylation of the HIC-1 candidate tumor suppressor gene in human breast cancer.". Oncogene 16 (16): 2159–64. doi:10.1038/sj.onc.1201976. PMID 9572497. 
• Deltour S, Guerardel C, Stehelin D, Leprince D (1999). "The carboxy-terminal end of the candidate tumor suppressor gene HIC-1 is phylogenetically conserved.". Biochim. Biophys. Acta 1443 (1-2): 230–2. PMID 9838134. 
• Deltour S, Guerardel C, Leprince D (2000). "Recruitment of SMRT/N-CoR-mSin3A-HDAC-repressing complexes is not a general mechanism for BTB/POZ transcriptional repressors: the case of HIC-1 and gammaFBP-B.". Proc. Natl. Acad. Sci. U.S.A. 96 (26): 14831–6. doi:10.1073/pnas.96.26.14831. PMC 24733. PMID 10611298. 
• Guerardel C, Deltour S, Pinte S, et al. (2001). "Identification in the human candidate tumor suppressor gene HIC-1 of a new major alternative TATA-less promoter positively regulated by p53.". J. Biol. Chem. 276 (5): 3078–89. doi:10.1074/jbc.M008690200. PMID 11073960. 
• Deltour S, Pinte S, Guérardel C, Leprince D (2001). "Characterization of HRG22, a human homologue of the putative tumor suppressor gene HIC1.". Biochem. Biophys. Res. Commun. 287 (2): 427–34. doi:10.1006/bbrc.2001.5624. PMID 11554746. 
• Deltour S, Pinte S, Guerardel C, et al. (2002). "The human candidate tumor suppressor gene HIC1 recruits CtBP through a degenerate GLDLSKK motif.". Mol. Cell. Biol. 22 (13): 4890–901. doi:10.1128/MCB.22.13.4890-4901.2002. PMC 133903. PMID 12052894. 
• Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932. 
• Cardoso C, Leventer RJ, Ward HL, et al. (2003). "Refinement of a 400-kb critical region allows genotypic differentiation between isolated lissencephaly, Miller-Dieker syndrome, and other phenotypes secondary to deletions of 17p13.3.". Am. J. Hum. Genet. 72 (4): 918–30. doi:10.1086/374320. PMC 1180354. PMID 12621583. 
• Rathi A, Virmani AK, Harada K, et al. (2004). "Aberrant methylation of the HIC1 promoter is a frequent event in specific pediatric neoplasms.". Clin. Cancer Res. 9 (10 Pt 1): 3674–8. PMID 14506157. 
• Waha A, Waha A, Koch A, et al. (2004). "Epigenetic silencing of the HIC-1 gene in human medulloblastomas.". J. Neuropathol. Exp. Neurol. 62 (11): 1192–201. PMID 14656076. 
• Lindsey JC, Lusher ME, Anderton JA, et al. (2004). "Identification of tumour-specific epigenetic events in medulloblastoma development by hypermethylation profiling.". Carcinogenesis 25 (5): 661–8. doi:10.1093/carcin/bgh055. PMID 14688019. 
• Pinte S, Guérardel C, Deltour-Balerdi S, et al. (2004). "Identification of a second G-C-rich promoter conserved in the human, murine and rat tumor suppressor genes HIC1.". Oncogene 23 (22): 4023–31. doi:10.1038/sj.onc.1207504. PMID 15007385. 
• Pinte S, Stankovic-Valentin N, Deltour S, et al. (2004). "The tumor suppressor gene HIC1 (hypermethylated in cancer 1) is a sequence-specific transcriptional repressor: definition of its consensus binding sequence and analysis of its DNA binding and repressive properties.". J. Biol. Chem. 279 (37): 38313–24. doi:10.1074/jbc.M401610200. PMID 15231840. 
• Chen W, Cooper TK, Zahnow CA, et al. (2004). "Epigenetic and genetic loss of Hic1 function accentuates the role of p53 in tumorigenesis.". Cancer Cell 6 (4): 387–98. doi:10.1016/j.ccr.2004.08.030. PMID 15488761. 
• Britschgi C, Rizzi M, Grob TJ, et al. (2006). "Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1.". Oncogene 25 (14): 2030–9. doi:10.1038/sj.onc.1209240. PMID 16301995. 
• Valenta T, Lukas J, Doubravska L, et al. (2006). "HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies.". EMBO J. 25 (11): 2326–37. doi:10.1038/sj.emboj.7601147. PMC 1478201. PMID 16724116. 
• Stankovic-Valentin N, Verger A, Deltour-Balerdi S, et al. (2006). "A L225A substitution in the human tumour suppressor HIC1 abolishes its interaction with the corepressor CtBP.". FEBS J. 273 (13): 2879–90. doi:10.1111/j.1742-4658.2006.05301.x. PMID 16762039. 

External links

• HIC1 protein, human at the US National Library of Medicine Medical Subject Headings (MeSH)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.