The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Angiotensin Type 2 Receptor Dephosphorylates Bcl-2 by Activating Mitogen-activated Protein Kinase Phosphatase-1 and Induces Apoptosis
Open accessAbstract
We examined the cellular and signaling mechanism of angiotensin II (Ang II) type 2 (AT2) receptor-induced apoptosis in PC12W (rat pheochromocytoma cell line) cells that express abundant AT2 receptor but not Ang II type 1 receptor. In these cells, nerve growth factor (NGF) inhibited the internucleosomal DNA fragmentation induced by serum depletion, whereas Ang II antagonized this NGF cell survival action and induced apoptosis. We studied the mechanism of NGF and AT2 receptor interaction on apoptosis by examining their effects on the survival factor Bcl-2. AT2 receptor activation did affect intracellular Bcl-2 protein levels. Bcl-2 phosphorylation was stimulated by NGF, whereas AT2 receptor activation blocked this NGF effect. Pretreatment with antisense oligonucleotide of mitogen-activated protein (MAP) kinase phosphatase-1 enhanced the effects of NGF on MAP kinase activation and Bcl-2 phosphorylation but attenuated the inhibitory effects of AT2 receptor on MAP kinase, Bcl-2 phosphorylation, and apoptosis. Taken together, these results suggest that MAP kinase plays a critical role in inhibiting apoptosis by phosphorylating Bcl-2. The AT2 receptor inhibits MAP kinase activation, resulting in the inactivation of Bcl-2 and the induction of apoptosis.
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Cites
Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis
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Bcl-2 and the regulation of programmed cell death
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The mitogen-activated protein kinase signal transduction pathway
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Self-citationInactivation of Bcl-2 by phosphorylation.
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Cited by
The Angiotensin AT2 Receptor: From a Binding Site to a Novel Therapeutic Target
Steckelings, U. M., Widdop, R. E., Sturrock, E. D., Lubbe, L., Hussain, T., Kaschina, E., Unger, T., Hallberg, A., Carey, R. M., & Sumners, C. (2022) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000281 · Cited by 97
The frail renin–angiotensin system
Abadir, P. M. (2011) · Clinics in Geriatric Medicine · doi:10.1016/j.cger.2010.08.004 · Cited by 70
Wilms, H., Rosenstiel, P., Unger, T., Deuschl, G., & Lucius, R. (2005) · American Journal of Cardiovascular Drugs · doi:10.2165/00129784-200505040-00004 · Cited by 52
Metadata
- Authors
- Horiuchi, M., Hayashida, W., Kambe, T., Yamada, T., & Dzau, V. J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1997-07
- Volume
- 272
- Issue
- 30
- Pages
- 19022-19026
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2031647568
- Cited by
- 295
- References
- 37
- FWCI
- 10.35
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Horiuchi, M., Hayashida, W., Kambe, T., Yamada, T., & Dzau, V. J. (1997). Angiotensin Type 2 Receptor Dephosphorylates Bcl-2 by Activating Mitogen-activated Protein Kinase Phosphatase-1 and Induces Apoptosis. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.272.30.19022
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
