The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Suppression of apoptosis signal-regulating kinase 1-induced cell death by 14-3-3 proteins
Open accessAbstract
Apoptosis signal-regulating kinase 1 (ASK1) is a pivotal component of a signaling pathway induced by many death stimuli, including tumor necrosis factor α, Fas, and the anticancer drugs cisplatin and paclitaxel. Here we report that ASK1 proapoptotic activity is antagonized by association with 14-3-3 proteins. We found that ASK1 specifically bound 14-3-3 proteins via a site involving Ser-967 of ASK1. Interestingly, overexpression of 14-3-3 in HeLa cells blocked ASK1-induced apoptosis whereas disruption of the ASK1/14-3-3 interaction dramatically accelerated ASK1-induced cell death. Targeting of ASK1 by a 14-3-3-mediated survival pathway may provide a novel mechanism for the suppression of apoptosis.
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Cited by
Reactive oxygen species, cellular redox systems, and apoptosis
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14-3-3 proteins in the nervous system
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JNK promotes Bax translocation to mitochondria through phosphorylation of 14‐3‐3 proteins
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The ASK1-MAP Kinase Cascades in Mammalian Stress Response
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Metadata
- Authors
- Zhang, L., Chen, J., & Fu, H.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-07-20
- Volume
- 96
- Issue
- 15
- Pages
- 8511-8515
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2008872627
- Cited by
- 351
- References
- 43
- FWCI
- 4.46
- Type
- journal article
- Language
- en
- Open access
- green
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- Zhang, L., Chen, J., & Fu, H. (1999). Suppression of apoptosis signal-regulating kinase 1-induced cell death by 14-3-3 proteins. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.15.8511
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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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