The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Beclin 1 cleavage by caspase-3 inactivates autophagy and promotes apoptosis
Open accessAbstract
Autophagy and apoptosis are both highly regulated biological processes that play essential roles in tissue homeostasis, development and diseases. Autophagy is also described as a mechanism of death pathways, however, the precise mechanism of how autophagy links to cell death remains to be fully understood. Beclin 1 is a dual regulator for both autophagy and apoptosis. In this study we found that Beclin 1 was a substrate of caspase-3 with two cleavage sites at positions 124 and 149, respectively. Furthermore, the autophagosome formation occurred, followed by the appearance of morphological hallmarks of apoptosis after staurosporine treatment. The cleavage products of Beclin 1 reduced autophagy and promoted apoptosis in HeLa cells and the cells in which Beclin 1 was stably knocked down by specific shRNA. In addition, the cleavage of Beclin 1 resulted in abrogating the interaction between Bcl-2 with Beclin 1, which could be blocked by z-VAD-fmk. Thus, our results suggest that the cleavage of Beclin 1 by caspase-3 may contribute to inactivate autophagy leading towards augmented apoptosis.
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Cites
Autophagy in the Pathogenesis of Disease
Levine, B., & Kroemer, G. (2008) · Cell · doi:10.1016/j.cell.2007.12.018 · Cited by 7,069
Role of Bcl-2 family proteins in a non-apoptotic programmed cell death dependent on autophagy genes
Shimizu, S., Kanaseki, T., Mizushima, N., Mizuta, T., Arakawa-Kobayashi, S., Thompson, C. B., & Tsujimoto, Y. (2004) · Nature Cell Biology · doi:10.1038/ncb1192 · Cited by 1,358
Zalckvar, E., Berissi, H., Mizrachy, L., Idelchuk, Y., Koren, I., Eisenstein, M., Sabanay, H., Pinkas‐Kramarski, R., & Kimchi, A. (2009) · The EMBO Reports · doi:10.1038/embor.2008.246 · Cited by 592
Dual Role of JNK1-mediated phosphorylation of Bcl-2 in autophagy and apoptosis regulation
Wei, Y., Sinha, S. C., & Levine, B. (2008) · Autophagy · doi:10.4161/auto.6788 · Cited by 424 · cited 2×
“The starvation-indcued activation of JNK1 can cause multi-site phosphorylation in the between BH4 and BH3 domain of Bcl-2, which leads to disrupt the interaction of Bcl-2 and Beclin 1 (Wei et al., 2008a, b; Pattingre et al., 2009).”
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Cited by
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).
Klionsky, D. J., Abdelmohsen, K., Abe, A., Abedin, M. J., Abeliovich, H., Acevedo Arozena, A., Adachi, H., Adams, C. M., Adams, P. D., Adeli, K., et al. (2016) · Autophagy · doi:10.1080/15548627.2015.1100356 · Cited by 5,894
Self-citationGuidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., et al. (2021) · Autophagy · doi:10.1080/15548627.2020.1797280 · Cited by 2,897
Self-citationOld, new and emerging functions of caspases
Shalini, S., Dorstyn, L., Dawar, S., & Kumar, S. (2015) · Cell Death & Differentiation · doi:10.1038/cdd.2014.216 · Cited by 1,267
Autophagy-dependent cell death
Denton, D., & Kumar, S. (2019) · Cell Death & Differentiation · doi:10.1038/s41418-018-0252-y · Cited by 777
Doherty, J., & Baehrecke, E. H. (2018) · Nature Cell Biology · doi:10.1038/s41556-018-0201-5 · Cited by 624
Metadata
- Authors
- Zhu, Y., Zhao, L., Liu, L., Gao, P., Tian, W., Wang, X., Jin, H., Xu, H., & Chen, Q.
- Venue
- Protein & Cell
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-05
- Volume
- 1
- Issue
- 5
- Pages
- 468-477
- ISSN
- 1674-800X (ISSN-L)
- 1674-8018
- OpenAlex
- W1983467638
- Cited by
- 254
- References
- 4
- FWCI
- 7.13
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Zhu, Y., Zhao, L., Liu, L., Gao, P., Tian, W., Wang, X., Jin, H., Xu, H., & Chen, Q. (2010). Beclin 1 cleavage by caspase-3 inactivates autophagy and promotes apoptosis. Protein & Cell. https://doi.org/10.1007/s13238-010-0048-4
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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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