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Cited by 160

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Bcl-2 Prevents Caspase-independent Cell Death

Open access
Okuno, Shin-ichiro, Shimizu, Shigeomi, Ito, Toshinori, Nomura, Masaya, Hamada, Eisaku, Tsujimoto, Yoshihide, Matsuda, Hikaru·1998·Journal of Biological Chemistry

Abstract

Nitric oxide (NO) is implicated in apoptosis and has both cytotoxic and cytoprotective effects. Exogenous NO induced the death of PC12 and HeLa cells via a process showing features of both apoptosis and necrosis, with chromatin condensation, nuclear compaction, and mitochondrial swelling. Activation of caspases was not observed during NO-induced cell death. In addition, cell death was not inhibited by peptide caspase inhibitors or by expression of p35, a baculovirus-encoded caspase inhibitor, indicating that NO-induced cell death was independent of caspases. NO-induced cell death was enhanced by Bax expression in a caspase-independent manner and prevented by the anti-cell death protein Bcl-2. Although Bcl-2 has previously been shown to prevent cell death by inhibiting caspase activation, these results indicate that it can also prevent cell death via a caspase-independent mechanism.

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Metadata

Authors
Okuno, S.-I., Shimizu, S., Ito, T., Nomura, M., Hamada, E., Tsujimoto, Y., & Matsuda, H.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1998-12
Volume
273
Issue
51
Pages
34272-34277
ISSN
0021-9258 (ISSN-L)
OpenAlex
W1971602494
Cited by
160
References
1
FWCI
7.32
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Bcl-2 Prevents Caspase-independent Cell Death. https://app.cochat.ai/papers/10.1074/jbc.273.51.34272
The paper
Okuno, S.-I., Shimizu, S., Ito, T., Nomura, M., Hamada, E., Tsujimoto, Y., & Matsuda, H. (1998). Bcl-2 Prevents Caspase-independent Cell Death. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.273.51.34272

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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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