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Gene Ontology Classifications
hairy/enhancer-of-split related with YRPW motif 2

Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Hey2. (This text reflects annotations as of Tuesday, May 26, 2015.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the hairy and enhancer of split-related (HESR) family of basic helix-loop-helix (bHLH)-type transcription factors. The encoded protein forms homo- or hetero-dimers that localize to the nucleus and interact with a histone deacetylase complex to repress transcription. Expression of this gene is induced by the Notch signal transduction pathway. Two similar and redundant genes in mouse are required for embryonic cardiovascular development, and are also implicated in neurogenesis and somitogenesis. Alternatively spliced transcript variants have been found, but their biological validity has not been determined. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text based on GO annotations supported by structural data
Summary text for additional MGI annotations
  1. Chin MT et al. (2000) Cardiovascular basic helix loop helix factor 1, a novel transcriptional repressor expressed preferentially in the developing and adult cardiovascular system. J Biol Chem, 275:6381-7. (PubMed:10692439)
  2. Doetzlhofer A et al. (2009) Hey2 regulation by FGF provides a Notch-independent mechanism for maintaining pillar cell fate in the organ of Corti. Dev Cell, 16:58-69. (PubMed:19154718)
  3. Donovan J et al. (2002) Tetralogy of fallot and other congenital heart defects in hey2 mutant mice. Curr Biol, 12:1605. (PubMed:12372254)
  4. Fischer A et al. (2007) Combined loss of Hey1 and HeyL causes congenital heart defects because of impaired epithelial to mesenchymal transition. Circ Res, 100:856-63. (PubMed:17303760)
  5. Fischer A et al. (2004) The Notch target genes Hey1 and Hey2 are required for embryonic vascular development. Genes Dev, 18:901-11. (PubMed:15107403)
  6. Fischer A et al. (2005) Hey basic helix-loop-helix transcription factors are repressors of GATA4 and GATA6 and restrict expression of the GATA target gene ANF in fetal hearts. Mol Cell Biol, 25:8960-70. (PubMed:16199874)
  7. Garg V et al. (2005) Mutations in NOTCH1 cause aortic valve disease. Nature, 437:270-4. (PubMed:16025100)
  8. Heisig J et al. (2012) Target gene analysis by microarrays and chromatin immunoprecipitation identifies HEY proteins as highly redundant bHLH repressors. PLoS Genet, 8:e1002728. (PubMed:22615585)
  9. Iso T et al. (2001) HERP, a novel heterodimer partner of HES/E(spl) in Notch signaling. Mol Cell Biol, 21:6080-9. (PubMed:11486045)
  10. Jalali A et al. (2011) HeyL promotes neuronal differentiation of neural progenitor cells. J Neurosci Res, 89:299-309. (PubMed:21259317)
  11. Kanno K et al. (2011) Differential effects of the HESR/HEY transcription factor family on dopamine transporter reporter gene expression via variable number of tandem repeats. J Neurosci Res, 89:562-75. (PubMed:21290414)
  12. Kathiriya IS et al. (2004) Hairy-related transcription factors inhibit GATA-dependent cardiac gene expression through a signal-responsive mechanism. J Biol Chem, 279:54937-43. (PubMed:15485867)
  13. Koibuchi N et al. (2007) CHF1/Hey2 plays a pivotal role in left ventricular maturation through suppression of ectopic atrial gene expression. Circ Res, 100:850-5. (PubMed:17332425)
  14. Kokubo H et al. (2004) Targeted disruption of hesr2 results in atrioventricular valve anomalies that lead to heart dysfunction. Circ Res, 95:540-7. (PubMed:15297376)
  15. Kokubo H et al. (2005) Mouse hesr1 and hesr2 genes are redundantly required to mediate Notch signaling in the developing cardiovascular system. Dev Biol, 278:301-9. (PubMed:15680351)
  16. Kokubo H et al. (2007) Hesr1 and Hesr2 regulate atrioventricular boundary formation in the developing heart through the repression of Tbx2. Development, 134:747-55. (PubMed:17259303)
  17. Li S et al. (2008) Hey2 functions in parallel with Hes1 and Hes5 for mammalian auditory sensory organ development. BMC Dev Biol, 8:20. (PubMed:18302773)
  18. Liu Y et al. (2010) The bHLH transcription factor CHF1/Hey2 regulates susceptibility to apoptosis and heart failure after pressure overload. Am J Physiol Heart Circ Physiol, 298:H2082-92. (PubMed:20382855)
  19. Maier MM et al. (2000) Comparative analysis of the human and mouse Hey1 promoter: Hey genes are new Notch target genes. Biochem Biophys Res Commun, 275:652-60. (PubMed:10964718)
  20. Nakagawa O et al. (2000) Members of the HRT family of basic helix-loop-helix proteins act as transcriptional repressors downstream of Notch signaling. Proc Natl Acad Sci U S A, 97:13655-60. (PubMed:11095750)
  21. Tang Y et al. (2008) Hairy-related transcription factors inhibit Notch-induced smooth muscle alpha-actin expression by interfering with Notch intracellular domain/CBF-1 complex interaction with the CBF-1-binding site. Circ Res, 102:661-8. (PubMed:18239137)
  22. Tokuzawa Y et al. (2010) Id4, a new candidate gene for senile osteoporosis, acts as a molecular switch promoting osteoblast differentiation. PLoS Genet, 6:e1001019. (PubMed:20628571)
  23. Watanabe T et al. (2010) Transcription factor CHF1/Hey2 regulates coronary vascular maturation. Mech Dev, 127:418-27. (PubMed:20619341)
  24. Xiang F et al. (2006) Transcription factor CHF1/Hey2 suppresses cardiac hypertrophy through an inhibitory interaction with GATA4. Am J Physiol Heart Circ Physiol, 290:H1997-2006. (PubMed:16603706)

Go Annotations in Tabular Form (Text View) (GO Graph)

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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IAS Inferred from ancestral sequence
  IBA Inferred from biological aspect of ancestor
  IBD Inferred from biological aspect of descendant
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IKR Inferred from key residues
  IMP Inferred from mutant phenotype
  IMR Inferred from missing residues
  IPI Inferred from physical interaction
  IRD Inferred from rapid divergence
  ISS Inferred from sequence or structural similarity
  ISO Inferred from sequence orthology
  ISA Inferred from sequence alignment
  ISM Inferred from sequence model
  NAS Non-traceable author statement
  ND No biological data available
  RCA Reviewed computational analysis
  TAS Traceable author statement


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