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Gene Review

Aes  -  amino-terminal enhancer of split

Rattus norvegicus

Synonyms: Amino enhancer of split, Amino-terminal enhancer of split, Esp1, Grg, Grg-5, ...
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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].


  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]
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