The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

Aes  -  amino-terminal enhancer of split

Rattus norvegicus

Synonyms: Amino enhancer of split, Amino-terminal enhancer of split, Esp1, Grg, Grg-5, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Aes

 

High impact information on Aes

  • The hydrodynamic properties of in vitro translated R-esp1 and R-esp2 proteins indicate that they do not stably self-associate or form heterodimers [2].
  • A model is presented for the possible role of the R-esp1 protein in the negative regulation of Enhancer of split proteins containing WD-40 repeats [2].
  • Overexpression of R-esp1 promotes cell survival even in the absence of NGF and, conversely, it is reduced by antisense-mediated inhibition of R-esp1 expression [3].
  • Therefore, we studied the influence of R-esp1 on nerve growth factor (NGF)-induced cell survival of PC12 cells [3].
  • This suggests that 17 beta-estradiol stimulates the expression of the ESP1 gene in the brain of both gender [1].
 

Biological context of Aes

  • The conservation of primary structure suggests a role of ESP1 peptide in oxygen consumption [1].
  • RESULTS: We identified several amino acid motifs that had high binding affinity to SB-236057-biotin conjugates, one with 100% sequence homology to a region of r-esp1, one of the Groucho homologs transcribed by the enhancer of split complex (En[spl]C) [4].
 

Anatomical context of Aes

  • R-esp1 mRNA was localized along the axis and antisense inhibition produced similar somite malformations as SB-236057 did [4].

References

  1. Characterization of an estradiol-stimulated mRNA in the brain of adult male rats. Nalik, P., Panayotova-Heiermann, M., Pongs, O. Mol. Cell. Endocrinol. (1989) [Pubmed]
  2. A rat homolog of the Drosophila enhancer of split (groucho) locus lacking WD-40 repeats. Schmidt, C.J., Sladek, T.E. J. Biol. Chem. (1993) [Pubmed]
  3. R-esp1, a rat homologue of drosophila groucho, is differentially expressed after optic nerve crush and mediates NGF-induced survival of PC12 cells. Arndt, M., Bank, U., Frank, K., Sabel, B.A., Ansorge, S., Lendeckel, U. FEBS Lett. (1999) [Pubmed]
  4. Evidence for a molecular mechanism of teratogenicity of SB-236057, a 5-HT1B receptor inverse agonist that alters axial formation. Augustine-Rauch, K.A., Zhang, Q.J., Leonard, J.L., Chadderton, A., Welsh, M.J., Rami, H.K., Thompson, M., Gaster, L., Wier, P.J. Birth defects research. Part A, Clinical and molecular teratology. (2004) [Pubmed]
 
WikiGenes - Universities