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Gene Review

Id3  -  inhibitor of DNA binding 3

Rattus norvegicus

Synonyms: DNA-binding protein inhibitor ID-3, Id-3, Inhibitor of DNA binding 3, Inhibitor of differentiation 3
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Disease relevance of Id3

  • RESULTS: The Id3 gene was expressed in the rapidly growing otocyst on embryonic Day 12 and specifically in the fundamental structures of the cochlea, e.g. the organ of Corti, spiral ganglions and stria vascularis, on postnatal Day 1 [1].
  • Adenovirus-mediated overexpression of these Id3 isoforms in cultured rat aortic SMCs revealed that infection of SMCs with an adenovirus overexpressing Id3a (in contrast to Id3) resulted in a significant decrease in cell number versus AdLacZ-infected cells [2].

Psychiatry related information on Id3


High impact information on Id3

  • Regulation of Id3 cell cycle function by Cdk-2-dependent phosphorylation [4].
  • Cdk2-dependent phosphorylation therefore provides a switch during late G1-to-S phase that both nullifies an early G1 cell cycle regulatory function of Id3 and modulates its target bHLH specificity [4].
  • We now show that an analogous cell-cycle-regulated phosphorylation of Id3 alters the specificity of Id3 for abrogating both E-box-dependent bHLH homo- or heterodimer complex formation in vitro and E-box-dependent reporter gene function in vivo [4].
  • However, at this time, Mash1, Math3, and Id3 expression are all concentrated in the area that specifically gives rise to granule cells and dentate precursor cells [5].
  • In contrast, Id3a stimulates SMC apoptosis and inhibits endogenous Id3 production [6].

Biological context of Id3


Anatomical context of Id3

  • We demonstrate that Id3 is expressed early in lesion formation when the proliferative index of the neointima is highest and that Id3 promotes smooth muscle cell (SMC) proliferation and S-phase entry and inhibits transcription of the cell-cycle inhibitor p21(Cip1) [6].
  • CONCLUSION: The Id3 gene is expressed in the developing cochlear tissue and participates in the development of cochlear progenitor hair cells during the embryonic stage [1].
  • The effects of Id3 on primary cultures of otocyst epithelial cells and a progenitor hair cell line (OT12) were studied using specific antisense oligonucleotides [1].
  • Unlike Id3, Id3a mRNA was not detected in the normal rat carotid artery [2].
  • The rapid induction as part of the early response to axonal membranes and cytokines suggested that Id3 is involved in myelin gene repression [8].

Associations of Id3 with chemical compounds

  • Intron retention generates a novel Id3 isoform that inhibits vascular lesion formation [6].
  • OBJECTIVES: Inhibitor of differentiation (Id3) is an important transcription factor expressed in the cochlear tissue and progenitor hair cells [1].
  • The data identified novel androgen-regulated genes (e.g. Id1, Id3, IL-6, IGF-binding protein-2 and -3, and JunB) [9].
  • Expression of the helix-loop-helix proteins Id1, Id2 and Id3 was specifically reduced by NGF and this effect was blocked in 5-azacytidine-treated cells, concomitant with the inhibition of NGF-induced neuronal differentiation [10].
  • CONCLUSIONS: Ang II induces proliferation of VSMCs via production of superoxide, which enhances the expression of Id3 [7].

Regulatory relationships of Id3

  • Ang II, X/XO, and overexpression of sense Id3 downregulated protein expression of p21(WAF1/Cip1), p27(Kip1), and p53 [7].

Other interactions of Id3


Analytical, diagnostic and therapeutic context of Id3


  1. Characterization of inhibitor of differentiation (Id3) gene expression in the developing cochlear tissue of rats. Ozeki, M., Schlentz, E.P., Lin, J. Acta Otolaryngol. (2005) [Pubmed]
  2. Vascular injury induces posttranscriptional regulation of the Id3 gene: cloning of a novel Id3 isoform expressed during vascular lesion formation in rat and human atherosclerosis. Matsumura, M.E., Li, F., Berthoux, L., Wei, B., Lobe, D.R., Jeon, C., Hammarskjöld, M.L., McNamara, C.A. Arterioscler. Thromb. Vasc. Biol. (2001) [Pubmed]
  3. Thyroid hormone, retinoic acid, and testosterone suppress proliferation and induce markers of differentiation in cultured rat sertoli cells. Buzzard, J.J., Wreford, N.G., Morrison, J.R. Endocrinology (2003) [Pubmed]
  4. Regulation of Id3 cell cycle function by Cdk-2-dependent phosphorylation. Deed, R.W., Hara, E., Atherton, G.T., Peters, G., Norton, J.D. Mol. Cell. Biol. (1997) [Pubmed]
  5. Unique expression patterns of cell fate molecules delineate sequential stages of dentate gyrus development. Pleasure, S.J., Collins, A.E., Lowenstein, D.H. J. Neurosci. (2000) [Pubmed]
  6. Intron retention generates a novel Id3 isoform that inhibits vascular lesion formation. Forrest, S.T., Barringhaus, K.G., Perlegas, D., Hammarskjold, M.L., McNamara, C.A. J. Biol. Chem. (2004) [Pubmed]
  7. Identification of a novel redox-sensitive gene, Id3, which mediates angiotensin II-induced cell growth. Mueller, C., Baudler, S., Welzel, H., Böhm, M., Nickenig, G. Circulation (2002) [Pubmed]
  8. Reciprocal Id expression and myelin gene regulation in Schwann cells. Thatikunta, P., Qin, W., Christy, B.A., Tennekoon, G.I., Rutkowski, J.L. Mol. Cell. Neurosci. (1999) [Pubmed]
  9. Androgens regulate the immune/inflammatory response and cell survival pathways in rat ventral prostate epithelial cells. Asirvatham, A.J., Schmidt, M., Gao, B., Chaudhary, J. Endocrinology (2006) [Pubmed]
  10. The DNA methyltransferase inhibitor 5-azacytidine specifically alters the expression of helix-loop-helix proteins Id1, Id2 and Id3 during neuronal differentiation. Persengiev, S.P., Kilpatrick, D.L. Neuroreport (1997) [Pubmed]
  11. Id-1 expression defines a subset of vimentin/S-100beta-positive, GFAP-negative astrocytes in the adult rat pineal gland. Kofler, B., Bulleyment, A., Humphries, A., Carter, D.A. Histochem. J. (2002) [Pubmed]
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