ArticleCell death and differentiation2017
DR5 and caspase-8 are dispensable in ER stress-induced apoptosis.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- The regulatory role of post-translational modifications in the pathogenesis of ulcerative colitis.Molecular biology reports · 2026Review
- IL-10 attenuates metabolic dysfunction-associated steatotic liver disease via modulation of hepatic responses to lipotoxicity.JCI insight · 2026Article
- A novel MMP13 frameshift variant causes short stature via enhanced MMP13-HSPA5 interaction and activated endoplasmic reticulum stress.Clinical and translational medicine · 2026Article
- Peptide-Mediated Precise Intracellular Delivery of Bioactive Substances.International journal of nanomedicine · 2026Review
- Targeting proteostasis for cancer therapy: current advances, challenges, and future perspectives.Molecular cancer · 2025Review
- MDM2 inhibitor induces apoptosis in colon cancer cells through activation of the CHOP-DR5 pathway, independent of p53 phenotype.Frontiers in pharmacology · 2025Article
- Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Article
- Defining a Water-Soluble Formulation of Arachidonic Acid as a Novel Ferroptosis Inducer in Cancer Cells.Biomolecules · 2024Article
- IRE1 RNase controls CD95-mediated cell death.EMBO reports · 2024Article
- Review
- Evasion of host antioxidative response via disruption of NRF2 signaling in fatal Ehrlichia-induced liver injury.PLoS pathogens · 2023Article
- When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death.Cell death and differentiation · 2023Review
- Novel Formulation of Undecylenic Acid induces Tumor Cell Apoptosis.International journal of molecular sciences · 2022Article
- Review
- Stress-induced inflammation evoked by immunogenic cell death is blunted by the IRE1α kinase inhibitor KIRA6 through HSP60 targeting.Cell death and differentiation · 2022Article
- EGCG Enhances the Chemosensitivity of Colorectal Cancer to Irinotecan through GRP78-MediatedEndoplasmic Reticulum Stress.Journal of oncology · 2022Article
- Zinc(II) niflumato complex effects on MMP activity and gene expression in human endometrial cell lines.Scientific reports · 2021Article
- The stressosome, a caspase-8-activating signalling complex assembled in response to cell stress in an ATG5-mediated manner.Journal of cellular and molecular medicine · 2021Article
- Cooperative treatment effectiveness of ATR and HSP90 inhibition in Ewing's sarcoma cells.Cell & bioscience · 2021Article
Corrections and comments
- Commented on by
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum (ER) stress response constitutes cellular reactions triggered by a wide variety of stimuli that disturb folding of proteins, often leading to apoptosis. ER stress-induced apoptotic cell death is thought to be an important contributor to many human pathological conditions. The molecular mechanism of this apoptosis process has been highly controversial with both the receptor and the mitochondrial pathways being implicated. Using knockout mouse models and RNAi-mediated gene silencing in cell lines, our group and others had demonstrated the importance of the mitochondrial apoptotic pathway in ER stress-induced cell death, particularly the role of the pro-apoptotic BH3-only BCL-2 family members, BIM and PUMA. However, a recent report suggested a central role for the death receptor, DR5, activated in a ligand-independent manner, and the initiator caspase, caspase-8, in ER stress-induced cell death. This prompted us to re-visit our previous observations and attempt to reproduce the newly published findings. Here we report that the mitochondrial apoptotic pathway, activated by BH3-only proteins, is essential for ER stress-induced cell death and that, in contrast to the previous report, DR5 as well as caspase-8 are not required for this process.
Indexed as
Identifiers
What OpenQuestion holds
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.