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Gtf2ird1  -  general transcription factor II I repeat...

Mus musculus

Synonyms: 1700012P16Rik, Alb-c-myc line 166.8, Alb/c-myc line 166.8, BEN, Ben, ...
 
 
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Disease relevance of Gtf2ird1

 

High impact information on Gtf2ird1

  • MusTRD1/BEN has five or six direct repeats, each containing helix--loop--helix motifs, and, thus, belongs to the TFII-I family of transcription factors [2].
  • We have used a yeast one-hybrid screen in a search for transcription factors that bind to EE motifs and have isolated a novel murine DNA-binding protein, termed BEN (binding factor for early enhancer) [3].
  • 5. Several BEN-encoded polypeptides of different sizes ranging from 165 to 40 kDa were identified by Western blot analysis using BEN-specific polyclonal Abs [3].
  • The BEN gene produces several major transcripts (3.6, 4.4, and 5.9 kb) present in most adult tissues and shows discrete spatial and temporal domains of expression in areas of epithelial-mesenchymal interaction during mouse embryogenesis from E9.5 to E12 [3].
  • Overexpression of BEN in P19 cells represses the TGFbeta-mediated transcriptional activation of Gsc [4].
 

Biological context of Gtf2ird1

 

Anatomical context of Gtf2ird1

  • Using RT-PCR, we detected Gtf2i and Gtf2ird1 mRNA transcripts in unfertilized oocytes, which indicates the maternal expression of these genes [8].
  • BEN, at this stage, is expressed only in the cytoplasm of trophoblast cells, but not in the ICM [Gene Expr. Patterns, 2003; 3, 577-587] [8].
  • Dominant-negative and RNAi-mediated knockdown experiments indicate that BEN can both positively and negatively regulate IgH promoter activity, depending on the cell line [9].
 

Other interactions of Gtf2ird1

  • Comparison of the genomic DNA structure in wildtype and transgenic mice revealed that the transgene integration had induced an approximately 40-kb deletion, starting downstream of the Cyln2 gene and including the first exon of the Gtf2ird1 gene [1].
  • CONCLUSIONS: These studies indicate that a genomic rearrangement affecting Nid or Estm9 does not underlie bg [10].

References

  1. Integration of a c-myc transgene results in disruption of the mouse Gtf2ird1 gene, the homologue of the human GTF2IRD1 gene hemizygously deleted in Williams-Beuren syndrome. Durkin, M.E., Keck-Waggoner, C.L., Popescu, N.C., Thorgeirsson, S.S. Genomics (2001) [Pubmed]
  2. Repression of TFII-I-dependent transcription by nuclear exclusion. Tussié-Luna, M.I., Bayarsaihan, D., Ruddle, F.H., Roy, A.L. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  3. Isolation and characterization of BEN, a member of the TFII-I family of DNA-binding proteins containing distinct helix-loop-helix domains. Bayarsaihan, D., Ruddle, F.H. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  4. Positive and negative regulation of the transforming growth factor beta/activin target gene goosecoid by the TFII-I family of transcription factors. Ku, M., Sokol, S.Y., Wu, J., Tussie-Luna, M.I., Roy, A.L., Hata, A. Mol. Cell. Biol. (2005) [Pubmed]
  5. Genomic organization of the genes Gtf2ird1, Gtf2i, and Ncf1 at the mouse chromosome 5 region syntenic to the human chromosome 7q11.23 Williams syndrome critical region. Bayarsaihan, D., Dunai, J., Greally, J.M., Kawasaki, K., Sumiyama, K., Enkhmandakh, B., Shimizu, N., Ruddle, F.H. Genomics (2002) [Pubmed]
  6. Regulation of alternative splicing of Gtf2ird1 and its impact on slow muscle promoter activity. Tay, E.S., Guven, K.L., Subramaniam, N., Polly, P., Issa, L.L., Gunning, P.W., Hardeman, E.C. Biochem. J. (2003) [Pubmed]
  7. Multiple GTF2I-like repeats of general transcription factor 3 exhibit DNA binding properties. Evidence for a common origin as a sequence-specific DNA interaction module. Vullhorst, D., Buonanno, A. J. Biol. Chem. (2005) [Pubmed]
  8. The early embryonic expression of TFII-I during mouse preimplantation development. Enkhmandakh, B., Bitchevaia, N., Ruddle, F., Bayarsaihan, D. Gene Expr. Patterns (2004) [Pubmed]
  9. Regulation of immunoglobulin promoter activity by TFII-I class transcription factors. Tantin, D., Tussie-Luna, M.I., Roy, A.L., Sharp, P.A. J. Biol. Chem. (2004) [Pubmed]
  10. Positional cloning of the Chediak-Higashi syndrome gene: genetic mapping of the beige locus on mouse chromosome 13. Kingsmore, S.F., Barbosa, M.D., Tchernev, V.T., Detter, J.C., Lossie, A.C., Seldin, M.F., Holcombe, R.F. J. Investig. Med. (1996) [Pubmed]
 
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