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Celf1  -  CUGBP, Elav-like family member 1

Mus musculus

Synonyms: 1600010O03Rik, 50 kDa nuclear polyadenylated RNA-binding protein, AA407467, Brain protein F41, Bruno-like protein 2, ...
 
 
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Disease relevance of Cugbp1

 

High impact information on Cugbp1

 

Biological context of Cugbp1

  • Here we report that CUG-BP is one of a novel family of developmentally regulated RNA binding proteins that includes embryonically lethal abnormal vision-type RNA binding protein 3 (ETR-3) [6].
  • Overexpression of CUG triplet repeat-binding protein, CUGBP1, in mice inhibits myogenesis [2].
  • The ability of CUGBP1 to induce LIP translation during APR depends on phosphorylation of CUGBP1 [7].
  • In conclusion, oltipraz inhibits adipogenesis by promoting LIP production and activation, and the enhanced LIP production accompanies cytoplasmic translocation of CUGBP1 and its binding to the GC-rich region of C/EBPbeta mRNA [8].
 

Anatomical context of Cugbp1

  • Our data demonstrate that the interaction of CUGBP1 with the eIF2alpha enhances the association of CUGBP1 with ribosomes and correlates with increased translation of LIP in the liver after partial hepatectomy [9].
  • Complementary experiments demonstrate a tissue-specific distribution of NAPOR, CUG-BP, and other highly related proteins within the nervous system as assayed by probing forebrain and hindbrain nuclear extracts with monoclonal antibody, mAb 3B1 [10].
  • Induction of CUGBP1 binding activity in liver cytoplasm during APR is accompanied by the elevation of CUGBP1 binding activity on polysomes [7].
 

Associations of Cugbp1 with chemical compounds

  • Enhanced CCAAT/enhancer-binding protein beta-liver-enriched inhibitory protein production by Oltipraz, which accompanies CUG repeat-binding protein-1 (CUGBP1) RNA-binding protein activation, leads to inhibition of preadipocyte differentiation [8].
 

Other interactions of Cugbp1

  • Two CELF proteins, CUG-BP and ETR-3, are nuclear and cytoplasmic in embryonic heart but are down-regulated in adult heart concomitant with loss of exon inclusion [11].
  • Oltipraz enhanced cytoplasmic translocation and RNA binding of CUG repeat-binding protein-1 (CUGBP1) but not calreticulin, another RNA-binding protein that interacts with C/EBPbeta mRNA [8].

References

  1. Transgenic mice expressing CUG-BP1 reproduce splicing mis-regulation observed in myotonic dystrophy. Ho, T.H., Bundman, D., Armstrong, D.L., Cooper, T.A. Hum. Mol. Genet. (2005) [Pubmed]
  2. Overexpression of CUG triplet repeat-binding protein, CUGBP1, in mice inhibits myogenesis. Timchenko, N.A., Patel, R., Iakova, P., Cai, Z.J., Quan, L., Timchenko, L.T. J. Biol. Chem. (2004) [Pubmed]
  3. Cardiac tissue-specific repression of CELF activity disrupts alternative splicing and causes cardiomyopathy. Ladd, A.N., Taffet, G., Hartley, C., Kearney, D.L., Cooper, T.A. Mol. Cell. Biol. (2005) [Pubmed]
  4. Reversible model of RNA toxicity and cardiac conduction defects in myotonic dystrophy. Mahadevan, M.S., Yadava, R.S., Yu, Q., Balijepalli, S., Frenzel-McCardell, C.D., Bourne, T.D., Phillips, L.H. Nat. Genet. (2006) [Pubmed]
  5. Inactivation of CUG-BP1/CELF1 causes growth, viability, and spermatogenesis defects in mice. Kress, C., Gautier-Courteille, C., Osborne, H.B., Babinet, C., Paillard, L. Mol. Cell. Biol. (2007) [Pubmed]
  6. The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing. Ladd, A.N., Charlet, N., Cooper, T.A. Mol. Cell. Biol. (2001) [Pubmed]
  7. Translational induction of liver-enriched transcriptional inhibitory protein during acute phase response leads to repression of CCAAT/enhancer binding protein alpha mRNA. Welm, A.L., Mackey, S.L., Timchenko, L.T., Darlington, G.J., Timchenko, N.A. J. Biol. Chem. (2000) [Pubmed]
  8. Enhanced CCAAT/enhancer-binding protein beta-liver-enriched inhibitory protein production by Oltipraz, which accompanies CUG repeat-binding protein-1 (CUGBP1) RNA-binding protein activation, leads to inhibition of preadipocyte differentiation. Bae, E.J., Kim, S.G. Mol. Pharmacol. (2005) [Pubmed]
  9. RNA CUG-binding protein 1 increases translation of 20-kDa isoform of CCAAT/enhancer-binding protein beta by interacting with the alpha and beta subunits of eukaryotic initiation translation factor 2. Timchenko, N.A., Wang, G.L., Timchenko, L.T. J. Biol. Chem. (2005) [Pubmed]
  10. Region-specific alternative splicing in the nervous system: implications for regulation by the RNA-binding protein NAPOR. Zhang, W., Liu, H., Han, K., Grabowski, P.J. RNA (2002) [Pubmed]
  11. Dynamic balance between activation and repression regulates pre-mRNA alternative splicing during heart development. Ladd, A.N., Stenberg, M.G., Swanson, M.S., Cooper, T.A. Dev. Dyn. (2005) [Pubmed]
 
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