The DOI matches its Crossref record; 222 of the 222 references it cites were found in a registry or an index.
BH3-only proteins in apoptosis and beyond: an overview
Open accessAbstract
BH3-only BCL-2 family proteins are effectors of canonical mitochondrial apoptosis. They discharge their pro-apoptotic functions through BH1–3 pro-apoptotic proteins such as BAX and BAK, while their activity is suppressed by BH1–4 anti-apoptotic BCL-2 family members. The precise mechanism by which BH3-only proteins mediate apoptosis remains unresolved. The existing data are consistent with three mutually non-exclusive models (1) displacement of BH1–3 proteins from complexes with BH1–4 proteins; (2) direct interaction with and conformational activation of BH1–3 proteins; and (3) membrane insertion and membrane remodeling. The BH3-only proteins appear to play critical roles in restraining cancer and inflammatory diseases such as rheumatoid arthritis. Molecules that mimic the effect of BH3-only proteins are being used in treatments against these diseases. The cell death activity of a subclass of BH3-only members (BNIP3 and BNIP3L) is linked to cardiomyocyte loss during heart failure. In addition to their established role in apoptosis, several BH3-only members also regulate diverse cellular functions in cell-cycle regulation, DNA repair and metabolism. Several members are implicated in the induction of autophagy and autophagic cell death, possibly through unleashing of the BH3-only autophagic effector Beclin 1 from complexes with BCL-2/BCL-xL. The Chapters included in the current Oncogene Review issues provide in-depth discussions on various aspects of major BH3-only proteins.
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Cites
1 retracted
Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia
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RetractedBcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
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Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
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“A transcriptionindependent pathway of p53-dependent apoptosis was shown to include physical interaction between mitochondrial p53 and anti- (BCL-2, BCL-xL) and proapoptotic (BAX, BAK) members of the BCL-2 family proteins (Mihara et al., 2003; Chipuk et al., 2004; Leu et al., 2004).”
Background
Cited by
BCL-2 family proteins: changing partners in the dance towards death
Kale, J., Osterlund, E. J., & Andrews, D. W. (2018) · Cell Death & Differentiation · doi:10.1038/cdd.2017.186 · Cited by 1,574
Apoptosis: A Target for Anticancer Therapy
Pfeffer, C., & Singh, A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19020448 · Cited by 1,542
Apoptosis (programmed cell death) and its signals - A review
Obeng, E. (2021) · Brazilian Journal of Biology · doi:10.1590/1519-6984.228437 · Cited by 513
Maiuri, M. C., Galluzzi, L., Morselli, E., Kepp, O., Malik, S. A., & Kroemer, G. (2010) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2009.12.001 · Cited by 502
Mitophagy in degenerative joint diseases
Sun, K., Jing, X., Guo, J., Yao, X., & Guo, F. (2021) · Autophagy · doi:10.1080/15548627.2020.1822097 · Cited by 459
Metadata
- Authors
- Lomonosova, E., & Chinnadurai, G.
- Venue
- Oncogene
- Published
- 2008-12
- Volume
- 27
- Issue
- S1
- Pages
- S2-S19
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1999653222
- Cited by
- 458
- References
- 222
- FWCI
- 8.69
- Type
- journal article
- Language
- en
- Open access
- green
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