The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
Interleukin 3-dependent survival by the Akt protein kinase
Open accessAbstract
Interleukin 3 (IL-3)-dependent survival of hematopoietic cells is known to rely on the activity of multiple signaling pathways, including a pathway leading to activation of phosphoinositide 3-kinase (PI 3-kinase), and protein kinase Akt is a direct target of PI 3-kinase. We find that Akt kinase activity is rapidly induced by the cytokine IL-3, suggesting a role for Akt in PI 3-kinase-dependent signaling in hematopoetic cells. Dominant-negative mutants of Akt specifically block Akt activation by IL-3 and interfere with IL-3-dependent proliferation. Overexpression of Akt or oncogenic v-akt protects 32D cells from apoptosis induced by IL-3 withdrawal. Apoptosis after IL-3 withdrawal is accelerated by expression of dominant-negative mutants of Akt, indicating that a functional Akt signaling pathway is necessary for cell survival mediated by the cytokine IL-3. Thus Akt appears to be an important mediator of anti-apoptotic signaling in this system.
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Cites
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Cited by
Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
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Regulation of Cell Death Protease Caspase-9 by Phosphorylation
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Metadata
- Authors
- Songyang, Z., Baltimore, D., Cantley, L. C., Kaplan, D. R., & Franke, T. F.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1997-10-14
- Volume
- 94
- Issue
- 21
- Pages
- 11345-11350
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1993205500
- Cited by
- 360
- References
- 56
- FWCI
- 13.39
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Songyang, Z., Baltimore, D., Cantley, L. C., Kaplan, D. R., & Franke, T. F. (1997). Interleukin 3-dependent survival by the Akt protein kinase. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.21.11345
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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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