The DOI matches its Crossref record; 121 of the 121 references it cites were found in a registry or an index.
Death versus survival: functional interaction between the apoptotic and stress-inducible heat shock protein pathways
Open accessAbstract
Induction of heat shock proteins (Hsps) following cellular damage can prevent apoptosis induced by both the intrinsic and the extrinsic pathways. The intrinsic pathway is characterized by mitochondrial outer membrane permeabilization (MOMP), cytochrome c release, apoptosome assembly, and caspase activation. Hsps promote cell survival by preventing MOMP or apoptosome formation as well as via regulation of Akt and JNK activities. Engagement of the TNF death receptors induces the extrinsic pathway that is characterized by Fas-associated death domain-dependent (FADD-dependent) caspase-8 activation or induction of NF-kappaB to promote cellular survival. Hsps can directly suppress proapoptotic signaling events or stabilizing elements of the NF-kappaB pathway to promote cellular survival.
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Cites
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Cited by
Mitochondrial membrane permeabilization in cell death
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The effects of oxidative stress on female reproduction: a review
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PINK1 Protects against Oxidative Stress by Phosphorylating Mitochondrial Chaperone TRAP1
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System-Wide Changes to SUMO Modifications in Response to Heat Shock
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Cell Death and Survival Assays
Kabakov, A. E., & Gabai, V. L. (2018) · Methods in Molecular Biology · doi:10.1007/978-1-4939-7477-1_9 · Cited by 156
Metadata
- Authors
- Beere, H. M.
- Venue
- Journal of Clinical Investigation
- Published
- 2005-10-01
- Volume
- 115
- Issue
- 10
- Pages
- 2633-2639
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2116902247
- Cited by
- 414
- References
- 121
- FWCI
- 12.33
- Type
- journal article
- Language
- en
- Open access
- bronze
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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.