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Gene Review

Gas1  -  growth arrest specific 1

Rattus norvegicus

 
 
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Disease relevance of Gas1

  • Overexpression of Gas1 in cultured hippocampal neurons and in human neuroblastoma NB69 cells produced a marked reduction in the number of viable cells [1].
  • We recently reported that the targeted expression of growth arrest specific 1 (Gas1) induces apoptosis in glioma cells [2].
 

High impact information on Gas1

  • The growth arrest-specific gene 1 (Gas1) protein has been proposed to function during development as an inhibitor of growth and a mediator of cell death and is also re-expressed in adult neurons during excitotoxic insult [3].
  • These results indicate that Gas1 is induced by activation of glutamate receptors and is part of the gene expression program directing neuronal death after mild excitotoxic insults [1].
  • While Gas1 does not directly interact with Bcl-2, OpIAP2 coimmunoprecipitates with Gas1 [1].
  • Importantly, Gas1-induced neuronal death was attenuated by coexpression of the human Bcl-2 protein or the baculoviral caspase inhibitor OpIAP2 [1].
  • BACKGROUND: Growth arrest-specific gene 6 (Gas6) is involved in a number of cell functions that include proliferation of vascular smooth muscle cells and mesangial cells [4].
 

Chemical compound and disease context of Gas1

  • While the identity of the caspase(s) responsible for Gas1-induced apoptosis in neurons has remained elusive, in C6 glioma cells, overexpression of Gas1 reproducibly activated caspase-3 [5].
 

Biological context of Gas1

  • Our aim here is to review the contributions of Gas1 and a few other selected genes and put them into a more comprehensive framework, though it may be speculative at times, of granule cell proliferation regulation [6].
  • Among them, the Growth arrest specific gene 1 (Gas1), a known negative regulator of the cell cycle, was shown to have profound influence on the production of the granule cells [6].
 

Anatomical context of Gas1

 

Associations of Gas1 with chemical compounds

  • Expression of Gas1 decreased glial proliferation and induced C6 cell apoptosis [5].

References

  1. Gas1 is induced during and participates in excitotoxic neuronal death. Mellström, B., Ceña, V., Lamas, M., Perales, C., Gonzalez, C., Naranjo, J.R. Mol. Cell. Neurosci. (2002) [Pubmed]
  2. Glial-specific retrovirally mediated gas1 gene expression induces glioma cell apoptosis and inhibits tumor growth in vivo. Zamorano, A., Mellström, B., Vergara, P., Naranjo, J.R., Segovia, J. Neurobiol. Dis. (2004) [Pubmed]
  3. Gas1 is related to the glial cell-derived neurotrophic factor family receptors alpha and regulates Ret signaling. Cabrera, J.R., Sanchez-Pulido, L., Rojas, A.M., Valencia, A., Mañes, S., Naranjo, J.R., Mellström, B. J. Biol. Chem. (2006) [Pubmed]
  4. Expression of growth arrest-specific gene 6 and its receptors in a rat model of chronic renal transplant rejection. Yin, J.L., Pilmore, H.L., Yan, Y.Q., McCaughan, G.W., Bishop, G.A., Hambly, B.D., Eris, J.M. Transplantation (2002) [Pubmed]
  5. Transcriptionally mediated gene targeting of gas1 to glioma cells elicits growth arrest and apoptosis. Zamorano, A., Lamas, M., Vergara, P., Naranjo, J.R., Segovia, J. J. Neurosci. Res. (2003) [Pubmed]
  6. Growth arrest specific gene 1: a fuel for driving growth in the cerebellum. Marques, G., Fan, C.M. Cerebellum (2002) [Pubmed]
  7. Apoptosis-associated gene expression in the corpus luteum of the rat. Guo, K., Wolf, V., Dharmarajan, A.M., Feng, Z., Bielke, W., Saurer, S., Friis, R. Biol. Reprod. (1998) [Pubmed]
  8. Growth arrest-specific 2 gene expression during patellar tendon healing. Lee, K.K., Cai, D.Q., Tang, M.K., Tsang, K.F., Kwong, W.H., Chow, P.H. Cells Tissues Organs (Print) (2003) [Pubmed]
 
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