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6 months of aerobic exercise can effectively prevent cardiomyocyte apoptosis in mice. It is an important way to effectively regulate Bcl-2, Bax expression and Bcl-2/Bax level of cardiomyocytes.
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data demonstrate that disruption of the beclin 1-BCL2 complex is an effective mechanism to increase autophagy, prevent premature ageing, improve healthspan and promote longevity in mammals
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Results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of age-related hearing loss in the auditory cortex.
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MiR-146a inhibits proliferation and induces apoptosis in murine osteoblastic MC3T3-E1 by regulating Bcl2
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The data revealed that autophagy is an important regulator of osteoblastic apoptosis through its interaction with Bax/Bcl2, and maintains the osteoblastic function of MC3T3E1 cells following GC exposure. In addition, these results indicated that the suppression of autophagy in OBs under chronic GC therapy may increase the prevalence of GCinduced osteoporosis and fragility fractures.
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Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation.
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The results suggest that SPK2 interacts with Bcl2 via its BH3 domain, thereby dissociating it from Beclin-1 and activating autophagy while protecting neurons against ischemic injury.
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The findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins, BCL2, Mcl1, and BCL2A1, rather than by a single anti-apoptotic protein.
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Bcl-2 is strongly expressed in the inner hair cells and spiral ganglion neurons of young mice. In addition, moderate Bcl-2 expression is also detected in the outer hair cells and in the neurons of the auditory cortex. A significant reduction of Bcl-2 expression in the cochlea or auditory cortex is also associated with elevated hearing thresholds and hair cell loss during aging.
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Bcl2 is the autophagy-related target of miR-449a.
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anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.
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Acute ethanol exposure induced autophagy-mediated heart toxicity and injury mainly through the ROS-JNK-Bcl-2 signaling pathway.
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Th17 cells are resistant to glucocorticoid-induced apoptosis and cytokine suppression, at least in part due to high levels of BCL-2. These findings support a role of Th17 cells in glucocorticoid-resistant inflammatory conditions such as certain endotypes of asthma.
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E2 protects skeletal myoblasts against apoptosis induced by H2 O2 modulating p53 and FoxO transcription factors and then their target genes Bcl-2, Bim, Puma, PERP, and MDM2, without affecting Noxa gene.
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Bcl-2 expression has a significant impact on the mineralogical content of enamel crystals of tooth structure
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The results suggest that CARP can protect against hypoxia-reperfusion induced cardiomyocyte apoptosis, possibly through increasing anti-apoptosis Bcl2 gene expression.
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This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 overexpression to promote B-cell lymphoma.
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an essential role for the binding of BCL2 to BIM in the survival of noncycling NK cells.
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LIGHT signalling pathway combined with IFN-gamma induces beta cells apoptosis via an NF-kappaB/Bcl2-dependent mitochondrial pathway.
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Bcl-2 was highly expressed in tubulointerstitial infiltrates in (NZB x NZW)F1 (NZB/NZW) lupus-prone mice.
