ArticleCellular and molecular life sciences : CMLS2013
Non-canonical function of Bax in stress-induced nuclear protein redistribution.
Article in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Nesprin-2 contains BH3-like motifs that can promote cell death.Cell death discovery · 2025Article
- Biochemical and neurophysiological effects of deficiency of the mitochondrial import protein TIMM50.eLife · 2024Article
- LINC complex protein nesprin-2 has pro-apoptotic activity via Bcl-2 family proteins.Cell death discovery · 2024Article
- Acute Genetic Damage Induced by Ethanol and Corticosterone Seems to Modulate Hippocampal Astrocyte Signaling.International journal of cell biology · 2024Article
- Apoptosis in megakaryocytes: Safeguard and threat for thrombopoiesis.Frontiers in immunology · 2022Review
- BCL-w: apoptotic and non-apoptotic role in health and disease.Cell death & disease · 2020Review
- The nuclear envelope: target and mediator of the apoptotic process.Cell death discovery · 2020Review
- Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins.Cell death discovery · 2020Article
- KPC1 alleviates hypoxia/reoxygenation-induced apoptosis in rat cardiomyocyte cells though BAX degradation.Journal of cellular physiology · 2019Article
- Simulated microgravity induces nuclear translocation of Bax and BCL-2 in glial cultured C6 cells.Heliyon · 2019Article
- Paeoniflorin induces G2/M cell cycle arrest and caspase-dependent apoptosis through the upregulation of Bcl-2 X-associated protein and downregulation of B-cell lymphoma 2 in human osteosarcoma cells.Molecular medicine reports · 2018Article
- Review
- Cellular stress induces Bax-regulated nuclear bubble budding and rupture followed by nuclear protein release.Nucleus (Austin, Tex.) · 2014Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bax and Bak (Bax/Bak) are essential pro-apoptotic proteins of the Bcl-2 family that trigger mitochondrial outer membrane permeabilization (MOMP) in a Bcl-2/Bcl-xL-inhibitable manner. We recently discovered a new stress-related function for Bax/Bak-regulation of nuclear protein redistribution (NPR) from the nucleus to cytoplasm. This effect was independent of Bax/Bak N-terminus exposure and not inhibited by Bcl-xL over-expression. Here, we studied the molecular mechanism governing this novel non-canonical response. Wild-type (WT) and mutant versions of Bax were re-expressed in Bax/Bak double-knockout mouse embryonic fibroblasts and their ability to promote NPR, apoptotic events, and changes in lamin A mobility was examined. Our results show that, in this system, Bax expression was sufficient to restore NPR such as in WT cells undergoing apoptosis. This activity of Bax was uncoupled from cytochrome c release from the mitochondria (indicative of MOMP) and required its membrane localization, α helices 5/6, and the Bcl-2 homology 3 (BH3) domain. Moreover, enrichment of Bax in the nuclear envelope by the so-called Klarsicht/ANC-1/Syne-1 homology domain effectively triggered NPR as in WT Bax, but without inducing MOMP or cell death. Bax-induced NPR was associated with impairment in lamin A mobility, implying a connection between these two nuclear envelope-associated events. Overall, the results indicate a new MOMP-independent, stress-induced Bax function on the nuclear envelope.
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