ArticleOncogene2000
Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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.
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Who cites it
85 citing papers in PubMed, 299 citations in OpenAlex.
- Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival-A Mathematical Study.International journal of molecular sciences · 2025Article
- Dolutegravir induces endoplasmic reticulum stress at the blood-brain barrier.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The C-terminal sequences of Bcl-2 family proteins mediate interactions that regulate cell death.The Biochemical journal · 2024Review
- Reappraisal of the fundamental mechanisms of the sHA14-1 molecule as a Bcl-2/Bcl-XL ligand in the context of anticancer therapy: A cell biological study.Journal of biological methods · 2024Article
- Inhibition of extracellular signal-regulated kinase downregulates endoplasmic reticulum stress-induced apoptosis and decreases brain injury in a cardiac arrest rat model.Physiological research · 2022Article
- Cellular Stress Pathways Are Linked to Acetamiprid-Induced Apoptosis in SH-SY5Y Neural Cells.Biology · 2021Article
- TOM20-mediated transfer of Bcl2 from ER to MAM and mitochondria upon induction of apoptosis.Cell death & disease · 2021Article
- Biological Pathways Associated with Neuroprogression in Bipolar Disorder.Brain sciences · 2021Article
- Induction of the Endoplasmic-Reticulum-Stress Response: MicroRNA-34a Targeting of the IRE1α-Branch.Cells · 2020Article
- Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction.Cell death & disease · 2019Article
- A mini review of fluoride-induced apoptotic pathways.Environmental science and pollution research international · 2018Review
- Mitochondrial dynamics in adaptive and maladaptive cellular stress responses.Nature cell biology · 2018Review
- Monocyte Response to DifferentToxins · 2018Article
- Tunicamycin induced endoplasmic reticulum stress promotes apoptosis of prostate cancer cells by activating mTORC1.Oncotarget · 2017Article
- Inflammatory diseases modelling in zebrafish.World journal of experimental medicine · 2016Article
- Crosstalk Between Endoplasmic Reticulum Stress, Oxidative Stress, and Autophagy: Potential Therapeutic Targets for Acute CNS Injuries.Molecular neurobiology · 2016Review
- Lost after translation: insights from pulmonary surfactant for understanding the role of alveolar epithelial dysfunction and cellular quality control in fibrotic lung disease.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Clic4, a novel protein that sensitizes β-cells to apoptosis.Molecular metabolism · 2015Article
- Caspase-12 mediates carbon tetrachloride-induced hepatocyte apoptosis in mice.World journal of gastroenterology · 2014Article
- Serum Bcl-2 Levels in Patients with β-Thalassemia Minor: A Pilot Study.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2014Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis involves mitochondrial steps such as the release of the apoptogenic factor cytochrome c which are effectively blocked by Bcl-2. Although Bcl-2 may have a direct action on the mitochondrial membrane, it also resides and functions on the endoplasmic reticulum (ER), and there is increasing evidence for a role of the ER in apoptosis regulation as well. Here we uncover a hitherto unrecognized, apoptotic crosstalk between the ER and mitochondria that is controlled by Bcl-2. After triggering massive ER dilation due to an inhibition of secretion, the drug brefeldin A (BFA) induces the release of cytochrome c from mitochondria in a caspase-8- and Bid-independent manner. This is followed by caspase-3 activation and DNA/nuclear fragmentation. Surprisingly, cytochrome c release by BFA is not only blocked by wild-type Bcl-2 but also by a Bcl-2 variant that is exclusively targeted to the ER (Bcl-2/cb5). Similar findings were obtained with tunicamycin, an agent interfering with N-linked glycosylations in the secretory system. Thus, apoptotic agents perturbing ER functions induce a novel crosstalk between the ER and mitochondria that can be interrupted by ER-based Bcl-2.
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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.