ArticleCell death discovery2020
Apoptotic stress induces Bax-dependent, caspase-independent redistribution of LINC complex nesprins.
Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263.Radiation oncology (London, England) · 2026Article
- Exploring the Role of Nesprin1 in isoproterenol-induced heart failure: Insights into pathogenesis and therapeutic implications.PloS one · 2026Article
- The role of endocannabinoid signaling in the cytoskeleton functionality in migrating neurons.Medical research archives · 2025Article
- Abnormalities of the endocannabinoid system produce piercing nuclear hernias in migrating cerebral neurons.iScience · 2025Article
- Nesprin-2 contains BH3-like motifs that can promote cell death.Cell death discovery · 2025Article
- Carbon monoxide-releasing molecule-3 ameliorates traumatic brain injury-induced cardiac dysfunctions via inhibition of pyroptosis and apoptosis.Molecular and cellular biochemistry · 2025Article
- Apoptosis-induced translocation of nesprin-2 from the nuclear envelope to mitochondria is associated with mitochondrial dysfunction.Nucleus (Austin, Tex.) · 2024Article
- The minimal membrane requirements for BAX-induced pore opening upon exposure to oxidative stress.Biophysical journal · 2024Article
- Calpain-1 weakens the nuclear envelope and promotes the release of neutrophil extracellular traps.Cell communication and signaling : CCS · 2024Article
- Prrx1-driven LINC complex disruption in vivo reduces osteoid deposition but not bone quality after voluntary wheel running.bioRxiv : the preprint server for biology · 2024Article
- LINC complex protein nesprin-2 has pro-apoptotic activity via Bcl-2 family proteins.Cell death discovery · 2024Article
- Prrx1-driven LINC complex disruption in vivo reduces osteoid deposition but not bone quality after voluntary wheel running.PloS one · 2024Article
- Mitochondrial Dynamics: Working with the Cytoskeleton and Intracellular Organelles to Mediate Mechanotransduction.Aging and disease · 2023Review
- Margetuximab conjugated-PEG-PAMAM G4 nano-complex: a smart nano-device for suppression of breast cancer.Biomedical engineering letters · 2022Article
- Apoptosis in Type 2 Diabetes: Can It Be Prevented? Hippo Pathway Prospects.International journal of molecular sciences · 2022Review
- Apoptosis in megakaryocytes: Safeguard and threat for thrombopoiesis.Frontiers in immunology · 2022Review
- Orchestration of Force Generation and Nuclear Collapse in Apoptotic Cells.International journal of molecular sciences · 2021Review
- Single-cell transcriptomic profiling reveals distinct mechanical responses between normal and diseased tendon progenitor cells.Cell reports. Medicine · 2021Article
- Anti-proliferative and anti-migratory properties of coffee diterpenes kahweol acetate and cafestol in human renal cancer cells.Scientific reports · 2021Article
- Targeted PEGylated Chitosan Nano-complex for Delivery of Sodium Butyrate to Prostate Cancer: An In Vitro Study.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
The canonical function of Bcl-2 family proteins is to regulate mitochondrial membrane integrity. In response to apoptotic signals the multi-domain pro-apoptotic proteins Bax and Bak are activated and perforate the mitochondrial outer membrane by a mechanism which is inhibited by their interaction with pro-survival members of the family. However, other studies have shown that Bax and Bak may have additional, non-canonical functions, which include stress-induced nuclear envelope rupture and discharge of nuclear proteins into the cytosol. We show here that the apoptotic stimuli cisplatin and staurosporine induce a Bax/Bak-dependent degradation and subcellular redistribution of nesprin-1 and nesprin-2 but not nesprin-3, of the linker of nucleoskeleton and cytoskeleton (LINC) complex. The degradation and redistribution were caspase-independent and did not occur in Bax/Bak double knockout (DKO) mouse embryo fibroblasts (MEFs). Re-expression of Bax in Bax/Bak DKO MEFs restored stress-induced redistribution of nesprin-2 by a mechanism which requires Bax membrane localization and integrity of the α helices 5/6, and the Bcl-2 homology 3 (BH3) domain. We found that nesprin-2 interacts with Bax in close proximity to perinuclear mitochondria in mouse and human cells. This interaction requires the mitochondrial targeting and N-terminal region but not the BH3 domain of Bax. Our results identify nesprin-2 as a Bax binding partner and also a new function of Bax in impairing the integrity of the LINC complex.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.