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Gene Review: 

Rap1GAP  -  Rap1 GTPase activating protein 1

Rattus norvegicus

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High impact information on Rap1GAP

  • The molecular function of the Tsc2 gene product (called "tuberin" in the human case) is not yet understood, although it contains a short amino acid sequence homologous to ras family GTPase-activating proteins (Rap1GAP) [1].
  • Upon TSH withdrawal, Rap1GAP undergoes a net increase in phosphorylation followed by proteasome-mediated degradation [2].
  • Glycogen synthase kinase 3beta (GSK3beta) phosphorylated Rap1GAP immunoprecipitated from thyroid cells, and GSK3beta inhibitors prevented phosphorylation and degradation of endogenous Rap1GAP [2].
  • Mutational analysis established a role for serine 525 in the regulation of Rap1GAP stability [2].
  • Transient expression of RalGDS-RBD or Rap1GAP to block the Rap1 pathway reduces the NGF-dependent neurite outgrowth in PC12-Shb cells [3].
 

Anatomical context of Rap1GAP

  • We now report that Rap1GAP protein levels are dynamically regulated in thyroid-stimulating hormone (TSH)-dependent thyroid cells [2].
 

Analytical, diagnostic and therapeutic context of Rap1GAP

References

  1. Presence of potent transcriptional activation domains in the predisposing tuberous sclerosis (Tsc2) gene product of the Eker rat model. Tsuchiya, H., Orimoto, K., Kobayashi, K., Hino, O. Cancer Res. (1996) [Pubmed]
  2. Thyroid-stimulating hormone/cAMP and glycogen synthase kinase 3beta elicit opposing effects on Rap1GAP stability. Tsygankova, O.M., Feshchenko, E., Klein, P.S., Meinkoth, J.L. J. Biol. Chem. (2004) [Pubmed]
  3. NGF-Dependent neurite outgrowth in PC12 cells overexpressing the Src homology 2-domain protein shb requires activation of the Rap1 pathway. Lu, L., Annerén, C., Reedquist, K.A., Bos, J.L., Welsh, M. Exp. Cell Res. (2000) [Pubmed]
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