World Library  
Flag as Inappropriate
Email this Article


Article Id: WHEBN0014065904
Reproduction Date:

Title: Tcf3  
Author: World Heritage Encyclopedia
Language: English
Subject: ID3 (gene), LYL1, ELK3, LMX1A, CBFA2T3
Collection: Transcription Factors
Publisher: World Heritage Encyclopedia


Transcription factor 3
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols  ; E2A; E47; ITF1; TCF-3; VDIR; bHLHb21
External IDs GeneCards:
RNA expression pattern
Species Human Mouse
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

Transcription factor 3 (E2A immunoglobulin enhancer-binding factors E12/E47), also known as TCF3, is a protein that in humans is encoded by the TCF3 gene.[1][2][3] TCF3 has been shown to directly enhance Hes1 (a well-known target of Notch signaling) expression.[4]


TCF3 has been shown to interact with ID3,[5][6] LYL1,[7] Twist transcription factor,[8] PCAF,[9] LMX1A,[10] LDB1,[11] ELK3,[12] CBFA2T3,[11] MyoD,[6][13] EP300,[9] CREB-binding protein,[9] MAPKAPK3,[14] Myogenin,[6][15] TAL1[11][16] and UBE2I.[17]


  1. ^ "Entrez Gene: TCF3". 
  2. ^ Henthorn P, McCarrick-Walmsley R, Kadesch T (February 1990). "Sequence of the cDNA encoding ITF-1, a positive-acting transcription factor". Nucleic Acids Res. 18 (3): 677.  
  3. ^ Kamps MP, Murre C, Sun XH, Baltimore D (February 1990). "A new homeobox gene contributes the DNA binding domain of the t(1;19) translocation protein in pre-B ALL". Cell 60 (4): 547–55.  
  4. ^ E proteins and Notch signaling cooperate to promote T cell lineage specification and commitment
  5. ^ Deed, R W; Jasiok M; Norton J D (April 1998). "Lymphoid-specific expression of the Id3 gene in hematopoietic cells. Selective antagonism of E2A basic helix-loop-helix protein associated with Id3-induced differentiation of erythroleukemia cells". J. Biol. Chem. (UNITED STATES) 273 (14): 8278–86.  
  6. ^ a b c Langlands, K; Yin X; Anand G; Prochownik E V (August 1997). "Differential interactions of Id proteins with basic-helix-loop-helix transcription factors". J. Biol. Chem. (UNITED STATES) 272 (32): 19785–93.  
  7. ^ Miyamoto, A; Cui X; Naumovski L; Cleary M L (May 1996). "Helix-loop-helix proteins LYL1 and E2a form heterodimeric complexes with distinctive DNA-binding properties in hematolymphoid cells". Mol. Cell. Biol. (UNITED STATES) 16 (5): 2394–401.  
  8. ^ El Ghouzzi, V; Legeai-Mallet L, Aresta S, Benoist C, Munnich A, de Gunzburg J, Bonaventure J (March 2000). "Saethre-Chotzen mutations cause TWIST protein degradation or impaired nuclear location". Hum. Mol. Genet. (ENGLAND) 9 (5): 813–9.  
  9. ^ a b c Bradney, Curtis; Hjelmeland Mark; Komatsu Yasuhiko; Yoshida Minoru; Yao Tso-Pang; Zhuang Yuan (January 2003). "Regulation of E2A activities by histone acetyltransferases in B lymphocyte development". J. Biol. Chem. (United States) 278 (4): 2370–6.  
  10. ^ Johnson, J D; Zhang W; Rudnick A; Rutter W J; German M S (July 1997). "Transcriptional synergy between LIM-homeodomain proteins and basic helix-loop-helix proteins: the LIM2 domain determines specificity". Mol. Cell. Biol. (UNITED STATES) 17 (7): 3488–96.  
  11. ^ a b c Goardon, Nicolas; Lambert Julie A; Rodriguez Patrick; Nissaire Philippe; Herblot Sabine; Thibault Pierre; Dumenil Dominique; Strouboulis John; Romeo Paul-Henri; Hoang Trang (January 2006). "ETO2 coordinates cellular proliferation and differentiation during erythropoiesis". EMBO J. (England) 25 (2): 357–66.  
  12. ^ Maira, S M; Wurtz J M; Wasylyk B (November 1996). "Net (ERP/SAP2) one of the Ras-inducible TCFs, has a novel inhibitory domain with resemblance to the helix-loop-helix motif". EMBO J. (ENGLAND) 15 (21): 5849–65.  
  13. ^ Maleki, S J; Royer C A; Hurlburt B K (June 1997). "MyoD-E12 heterodimers and MyoD-MyoD homodimers are equally stable". Biochemistry (UNITED STATES) 36 (22): 6762–7.  
  14. ^ Neufeld, B; Grosse-Wilde A; Hoffmeyer A; Jordan B W; Chen P; Dinev D; Ludwig S; Rapp U R (July 2000). "Serine/Threonine kinases 3pK and MAPK-activated protein kinase 2 interact with the basic helix-loop-helix transcription factor E47 and repress its transcriptional activity". J. Biol. Chem. (UNITED STATES) 275 (27): 20239–42.  
  15. ^ Chakraborty, T; Martin J F; Olson E N (September 1992). "Analysis of the oligomerization of myogenin and E2A products in vivo using a two-hybrid assay system". J. Biol. Chem. (UNITED STATES) 267 (25): 17498–501.  
  16. ^ Hsu, H L; Wadman I; Baer R (April 1994). "Formation of in vivo complexes between the TAL1 and E2A polypeptides of leukemic T cells".  
  17. ^ Huggins, G S; Chin M T; Sibinga N E; Lee S L; Haber E; Lee M E (October 1999). "Characterization of the mUBC9-binding sites required for E2A protein degradation". J. Biol. Chem. (UNITED STATES) 274 (40): 28690–6.  

Further reading

  • LeBrun DP (2004). "E2A basic helix-loop-helix transcription factors in human leukemia". Front. Biosci. 8: s206–22.  

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.