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Cited by 1,901

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Cell Survival Promoted by the Ras-MAPK Signaling Pathway by Transcription-Dependent and -Independent Mechanisms

Bonni, Azad, Brunet, Anne, West, Anne E., Datta, Sandeep Robert, Takasu, Mari A., Greenberg, Michael E.·1999·Science

Abstract

A mechanism by which the Ras–mitogen-activated protein kinase (MAPK) signaling pathway mediates growth factor–dependent cell survival was characterized. The MAPK-activated kinases, the Rsks, catalyzed the phosphorylation of the pro-apoptotic protein BAD at serine 112 both in vitro and in vivo. The Rsk-induced phosphorylation of BAD at serine 112 suppressed BAD-mediated apoptosis in neurons. Rsks also are known to phosphorylate the transcription factor CREB (cAMP response element–binding protein) at serine 133. Activated CREB promoted cell survival, and inhibition of CREB phosphorylation at serine 133 triggered apoptosis. These findings suggest that the MAPK signaling pathway promotes cell survival by a dual mechanism comprising the posttranslational modification and inactivation of a component of the cell death machinery and the increased transcription of pro-survival genes.

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Metadata

Authors
Bonni, A., Brunet, A., West, A. E., Datta, S. R., Takasu, M. A., & Greenberg, M. E.
Venue
Science
Published
1999-11-12
Volume
286
Issue
5443
Pages
1358-1362
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1976441097
Cited by
1,901
References
5
FWCI
39.26
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Cell Survival Promoted by the Ras-MAPK Signaling Pathway by Transcription-Dependent and -Independent Mechanisms. https://app.cochat.ai/papers/10.1126/science.286.5443.1358
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Bonni, A., Brunet, A., West, A. E., Datta, S. R., Takasu, M. A., & Greenberg, M. E. (1999). Cell Survival Promoted by the Ras-MAPK Signaling Pathway by Transcription-Dependent and -Independent Mechanisms. Science. https://doi.org/10.1126/science.286.5443.1358

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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