The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Growth retardation and increased apoptosis in mice with homozygous disruption of the akt1 gene
Open accessAbstract
The serine/threonine kinase Akt has been implicated in the control of cell survival and metabolism. Here we report the disruption of the most ubiquitously expressed member of the akt family of genes, akt1 , in the mouse. Akt1 −/− mice are viable but smaller when compared to wild-type littermates. In addition, the life span of Akt1 −/− mice, upon exposure to genotoxic stress, is shorter. However, Akt1 −/− mice do not display a diabetic phenotype. Increased spontaneous apoptosis in testes, and attenuation of spermatogenesis is observed in Akt1 −/− male mice. Increased spontaneous apoptosis is also observed in the thymi of Akt1 −/− mice, and Akt1 −/− thymocytes are more sensitive to apoptosis induced by γ-irradiation and dexamethasone. Finally, Akt1 −/− mouse embryo fibroblasts (MEFs) are more susceptible to apoptosis induced by TNF, anti-Fas, UV irradiation, and serum withdrawal.
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Cites
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Cellular survival: a play in three Akts
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p53 is required for radiation-induced apoptosis in mouse thymocytes
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Cited by
Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex
Sarbassov, D. D., Guertin, D. A., Ali, S. M., & Sabatini, D. M. (2005) · Science · doi:10.1126/science.1106148 · Cited by 6,216
AKT/PKB Signaling: Navigating the Network
Manning, B. D., & Toker, A. (2017) · Cell · doi:10.1016/j.cell.2017.04.001 · Cited by 3,772
Critical nodes in signalling pathways: insights into insulin action
Taniguchi, C. M., Emanuelli, B., & Kahn, C. R. (2006) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1837 · Cited by 2,760
Shiojima, I. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24682 · Cited by 939
Mutant PIK3CA promotes cell growth and invasion of human cancer cells.
Samuels, Y., Diaz, L. A., Schmidt-Kittler, O., Cummins, J. M., DeLong, L., Cheong, I., Rago, C., Huso, D. L., Lengauer, C., Kinzler, K. W., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.05.014 · Cited by 915
Metadata
- Authors
- Chen, W. S., Xu, P.-Z., Gottlob, K., Chen, M.-L., Sokol, K., Shiyanova, T., Roninson, I., Weng, W., Suzuki, R., Tobe, K., Kadowaki, T., & Hay, N.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-09-01
- Volume
- 15
- Issue
- 17
- Pages
- 2203-2208
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2140439371
- Cited by
- 928
- References
- 5
- Type
- posted content
- Language
- en
- Open access
- diamond
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- Chen, W. S., Xu, P.-Z., Gottlob, K., Chen, M.-L., Sokol, K., Shiyanova, T., Roninson, I., Weng, W., Suzuki, R., Tobe, K., Kadowaki, T., & Hay, N. (2001). Growth retardation and increased apoptosis in mice with homozygous disruption of the akt1 gene. Genes & Development. https://doi.org/10.1101/gad.913901
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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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