The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
The Phosphatidylinositol 3-Kinase (PI3K)-Akt Pathway Suppresses Bax Translocation to Mitochondria
Open accessAbstract
Bax, a proapoptotic member of the Bcl-2 family, localizes largely in the cytoplasm but redistributes to mitochondria in response to apoptotic stimuli, where it induces cytochrome c release. In this study, we show that the phosphatidylinositol 3-OH kinase (PI3K)-Akt pathway plays an important role in the regulation of Bax subcellular localization. We found that LY294002, a PI3K inhibitor, blocked the effects of serum to prevent Bax translocation to mitochondria and that expression of an active form of PI3K suppressed staurosporine-induced Bax translocation, suggesting that PI3K activity is essential for retaining Bax in the cytoplasm. In contrast, both U0126, a MEK inhibitor, and active MEK had little effect on Bax localization. In respect to downstream effectors of PI3K, we found that expression of active Akt, but not serum and glucocorticoid-induced protein kinase (SGK), suppressed staurosporine-induced translocation of Bax, whereas dominant negative Akt moderately promoted Bax translocation. Expression of Akt did not alter the levels of Bax, Bcl-2, Bcl-X(L), or phosphorylated JNK under the conditions used, suggesting that there were alternative mechanisms for Akt in the suppression of Bax translocation. Collectively, these results suggest that the PI3K-Akt pathway inhibits Bax translocation from cytoplasm to mitochondria and have revealed a novel mechanism by which the PI3K-Akt pathway promotes survival.
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Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
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Self-citationAkt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
Brunet, A., Bonni, A., Zigmond, M. J., Lin, M. Z., Juo, P., Hu, L. S., Anderson, M. J., Arden, K. C., Blenis, J., & Greenberg, M. E. (1999) · Cell · doi:10.1016/s0092-8674(00)80595-4 · Cited by 5,594
Cleavage of BID by Caspase 8 Mediates the Mitochondrial Damage in the Fas Pathway of Apoptosis
Li, H., Zhu, H., Xu, C.-J., & Yuan, J. (1998) · Cell · doi:10.1016/s0092-8674(00)81590-1 · Cited by 4,445
Cellular survival: a play in three Akts
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Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
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BCL-2 family members and the mitochondria in apoptosis
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Mitochondrial control of cell death
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(Patho)physiological Significance of the Serum- and Glucocorticoid-Inducible Kinase Isoforms
Lang, F., Böhmer, C., Palmada, M., Seebohm, G., Strutz-Seebohm, N., & Vallon, V. (2006) · Physiological Reviews · doi:10.1152/physrev.00050.2005 · Cited by 689
Rathmell, J. C., Fox, C. J., Plas, D. R., Hammerman, P. S., Cinalli, R. M., & Thompson, C. B. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.20.7315-7328.2003 · Cited by 572
JNK promotes Bax translocation to mitochondria through phosphorylation of 14‐3‐3 proteins
Tsuruta, F., Sunayama, J., Mori, Y., Hattori, S., Shimizu, S., Tsujimoto, Y., Yoshioka, K., Masuyama, N., & Gotoh, Y. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600194 · Cited by 556
Self-citationIschemic preconditioning protects by activating prosurvival kinases at reperfusion
Hausenloy, D. J., Tsang, A., Mocanu, M. M., & Yellon, D. M. (2005) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00374.2004 · Cited by 512
Kim, B.-J., Ryu, S.-W., & Song, B.-J. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m510644200 · Cited by 470
Metadata
- Authors
- Tsuruta, F., Masuyama, N., & Gotoh, Y.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-04
- Volume
- 277
- Issue
- 16
- Pages
- 14040-14047
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2013105209
- Cited by
- 383
- References
- 51
- FWCI
- 7.02
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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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