Bcl-2 proteins and mitochondria—Specificity in membrane targeting for death

Lindsay, Jennefer; Esposti, Mauro Degli; Gilmore, Andrew

doi:10.1016/j.bbamcr.2010.10.017

Cited by 301 publications

(257 citation statements)

References 97 publications

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“…Bcl-2 family proteins regulate mitochondrion-dependent apoptosis by influence on the permeability of MOM (29). Apoptosis-associated MOMP is known to require pro-apoptotic Bax-like proteins (in regulation of the formation of pores in the mitochondria) and anti-apoptotic Bcl-2-like proteins (functionally distinct from their role in mitochondrial morphogenesis) (30).…”

Section: Discussionmentioning

confidence: 99%

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Ye²,

Cai³

et al. 2011

Oncol Rep

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Abstract. The efficacy and safety of millimeter wave radiation has been proven for various types of malignant tumors. However, the mechanisms underlying effects of millimeter wave radiation on apoptosis are still unclear. The present study was undertaken to examine the effects of millimeter wave radiation on cell apoptosis and mitochondrial membrane potential, and to determine the molecular mechanism of millimeter wave radiation-induced apoptosis by investigating the expression of Bcl-2 family proteins (Bcl-2, Bax), caspase-9 and caspase-3 in SW1353 cells. We found that millimeter wave radiation suppressed the viability of SW1353 cells, demonstrating that millimeter wave radiation induced cell apoptosis and reduced cell viability in a time-dependent manner. Furthermore, we observed that treatment of cells with millimeter wave radiation significantly induced loss of mitochondrial membrane potential, upregulated proapoptotic Bax, caspase-9 and caspase-3, but did not significantly change levels of antiapoptotic Bcl-2. These data suggested that millimeter wave radiation may induce apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 cells.

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Section: Discussionmentioning

confidence: 99%

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Ye²,

Cai³

et al. 2011

Oncol Rep

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“…We have previously shown that PRL-induced BCLXL is needed for its pro-survival effect against DEX-induced cell death in INS-1 cells [26]. The BCL family of proteins is a major regulator of the intrinsic mitochondrial cell death pathway [43]. Considering that both DEX and GLT mediate their toxic effects through the intrinsic cell death pathway [44,45], it is not surprising that BCLXL, an anti-apoptotic member of the BCL family, is protective against both cell death inducers.…”

Section: Discussionmentioning

confidence: 99%

Lactogens protect rodent and human beta cells against glucolipotoxicity-induced cell death through Janus kinase‐2 (JAK2)/signal transducer and activator of transcription-5 (STAT5) signalling

et al. 2012

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Aims/hypothesis A leading cause of type 2 diabetes is a reduction in functional beta cell mass partly due to increased beta cell death, triggered by stressors such as glucolipotoxicity (GLT). This study evaluates the hypothesis that lactogens can protect beta cells against GLT and examines the mechanism behind the pro-survival effect. Methods The effect of exogenous treatment or endogenous expression of lactogens on GLT-induced beta cell death was examined in INS-1 cells, and in rodent and human islets. The mechanism behind the pro-survival effect of lactogens was determined using an inhibitor, siRNAs, a dominant negative (DN) mutant, and Cre-lox-mediated gene deletion analysis. Results Lactogens significantly protect INS-1 and primary rodent beta cells against GLT-induced cell death. The prosurvival effect of lactogens in rodent beta cells is mediated through activation of the Janus kinase-2 (JAK2)/signal transducer and activator of transcription-5 (STAT5) signalling pathway. Lactogen-induced increase in the anti-apoptotic B cell lymphoma-extra large (BCLXL) protein is required to mediate its pro-survival effects in both INS-1 cells and primary rodent beta cells. Most importantly, lactogens significantly protect human beta cells against GLT-induced cell death, and their prosurvival effect is also mediated through the JAK2/STAT5 pathway. Conclusions/interpretation These studies, together with previous work, clearly demonstrate the pro-survival nature of lactogens and identify the JAK2/STAT5 pathway as an important mediator of this effect in both rodent and human beta cells. Future studies will determine the effectiveness of this peptide in vivo in the pathophysiology of type 2 diabetes.

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“…Z designates a stop codon. Adapted from Lindsay et al (2011) Membrane binding properties of the C-terminal domain of Bcl-2 family proteins…”

Section: Mode 1 Inhibiɵonmentioning

confidence: 99%

Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization

et al. 2017

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Apoptosis is important in regulating cell death turnover and is mediated by the intrinsic and death receptor-based extrinsic pathways which converge at the mitochondrial outer membrane (MOM) leading to mitochondrial outer membrane permeabilization (MOMP). MOMP results in the release of apoptotic proteins that further activate the downstream pathway of apoptosis. Thus, tight regulation of MOMP is crucial in controlling apoptosis, and a lack of control may lead to tissue and organ malformation and the development of cancers. Despite a growing number of studies focusing on the structure and activity of the proteins involved in mediating MOMP, such as the Bcl-2 family proteins, the mechanism of MOMP is not well understood. In particular, the crucial role of the various structural properties and changes in lipid components of the MOM in mediating the recruitment and activation of different Bcl-2 proteins remains poorly understood. Furthermore, the factors that control the changes in mitochondrial membrane integrity from the initiation to the final disruption of MOM have yet to be clearly defined. In this review, we provide an overview of studies that focus on the mitochondrial membrane with a biophysical analysis of the interactions of the Bcl-2 proteins with the mitochondrial membrane.

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Bcl-2 proteins and mitochondria—Specificity in membrane targeting for death

Cited by 301 publications

References 97 publications

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Lactogens protect rodent and human beta cells against glucolipotoxicity-induced cell death through Janus kinase‐2 (JAK2)/signal transducer and activator of transcription-5 (STAT5) signalling

Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization

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