Bcl‐2 family proteins: The sentinels of the mitochondrial apoptosis pathway

Wong, Wendy Wei-Lynn; Puthalakath, Hamsa

doi:10.1002/iub.51

Cited by 164 publications

(118 citation statements)

References 85 publications

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“…While anti-apoptotic effect of Bcl-2 is through the inhibition of the release of Cytochromum C from mitochondria for Caspase activation [29][30][31], all three treated groups also exhibited an induction of Caspase protein and mRNA expression ( Figures 5 and 6). A relatively stronger induction of Caspase 3 was observed in the ACBP-L treated group, while a stronger induction of Caspase 8 was observed in the combinatory treated group ( Figure 5).…”

Section: Discussionmentioning

confidence: 96%

STAG2 is a Clinically Relevant Tumor Suppressor in Pancreatic Ductal Adenocarcinoma

2014

Cancer Cell Signaling

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Background: A great challenge of cancer chemotherapy is to eliminate cancer cells and concurrently maintain the quality of life (QOL) for cancer patients. Previously, we identified a novel anti-cancer bioactive peptide (ACBP), a peptide induced in goat spleen or liver following immunization with human gastric cancer protein extract. ACBP alone exhibited anti-tumor activity without measurable side effects. Thus, we hypothesize that ACBP and combined chemotherapy could improve the efficacy of treatment and lead to a better QOL.

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Section: Discussionmentioning

confidence: 96%

STAG2 is a Clinically Relevant Tumor Suppressor in Pancreatic Ductal Adenocarcinoma

2014

Cancer Cell Signaling

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“…Stress conditions influence the expression and location of Bcl-2 family proteins such as the pro-apoptotic Bax protein [15]. In certain situations, anti-apoptotic members of the Bcl-2 family such as inhibitor of apoptosis protein (IAP) may be involved in delaying apoptosis [16].…”

Section: Introductionmentioning

confidence: 99%

Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

Kim

Lee

et al. 2010

Eur J Immunol

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Although Helicobacter pylori infections of the gastric mucosa are characterized by the infiltration of inflammatory cells such as eosinophils, the responses of eosinophils to H. pylori vacuolating cytotoxin (VacA) have not been fully elucidated. This study investigates the role of VacA in the apoptosis of human eosinophils. We treated human eosinophils with purified H. pylori VacA and observed that induction of apoptosis is a relatively late event. Expression of cellular inhibitor of apoptosis protein (c-IAP)-2 was upregulated during the early period of VacA stimulation, and transfection with c-IAP2 siRNA augmented apoptotic cell death. VacA caused the translocation of cytoplasmic Bax to the mitochondria and increased cytochrome c release from mitochondria in eosinophils. Transfection of an EoL-1 eosinophil cell line with Bax siRNA decreased the release of cytochrome c and DNA fragmentation. Furthermore, apoptosis facilitated by Bax and cytochrome c was primarily regulated by p38 MAPK in VacA-treated eosinophils. These results suggest that the exposure of human eosinophils to H. pylori VacA induces the early upregulation of c-IAP2 and a relatively late apoptotic response, with the apoptosis progressing through a sequential pathway that includes p38 MAPK activation, Bax translocation, and cytochrome c release.

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“…Bcl-2 family members are the arbiters of the mitochondrial apoptotic pathway and decide whether a cell lives or dies [24] . This family includes anti-apoptotic and pro-apoptotic genes [25] .…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane protects primary cultures of cortical neurons against injury induced by oxygen-glucose deprivation/reoxygenation via antiapoptosis

Zhao

et al. 2012

Neurosci. Bull.

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Objective To determine whether sulforaphane (SFN) protects neurons against injury caused by oxygenglucose deprivation/reoxygenation (OGD/R) and, if so, to investigate the possible mechanisms. Methods Primary cultures of neurons were prepared from the cerebral cortex of 1-day-old Sprague-Dawley rats. On days 5-6 in vitro, the neurons were exposed to OGD for 1 h, followed by reoxygenation for 24 h. Cells were treated with 0, 0.1, 0.2, 0.5, 1, 2.5, or 5 µmol/L SFN, with or without 10 µmol/L LY294002, a PI3K-specific inhibitor, during OGD/R (a total of 25 h). After 24-h reoxygenation, MTT was used to assess viability and injury was assessed by Hoechst 33258/propidium iodide (PI) staining; immunofluorescence staining and Western blot were performed to detect molecular events associated with apoptosis. ResultsThe MTT assay showed that 1 µmol/L SFN significantly increased viability, and Hoechst 33258/PI staining showed that the numbers of injured neurons were reduced significantly in the SFN group. Furthermore, immunofluorescence staining and Western blot showed that SFN increased Bcl-2 and decreased cleaved caspase-3 levels. Moreover, LY294002 inhibited the phosphorylated-Akt expression evoked by SFN, decreased Bcl-2 expression and increased cleaved caspase-3 expression.Conclusion SFN protects neurons against injury from OGD/R and this effect may be partly associated with an antiapoptosis pathway.

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Bcl‐2 family proteins: The sentinels of the mitochondrial apoptosis pathway

Cited by 164 publications

References 85 publications

STAG2 is a Clinically Relevant Tumor Suppressor in Pancreatic Ductal Adenocarcinoma

STAG2 is a Clinically Relevant Tumor Suppressor in Pancreatic Ductal Adenocarcinoma

Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

Sulforaphane protects primary cultures of cortical neurons against injury induced by oxygen-glucose deprivation/reoxygenation via antiapoptosis

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