ArticleOncogene2005
Caspase-9 and effector caspases have sequential and distinct effects on mitochondria.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 45 citations in OpenAlex.
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- Plausible computational insights and new atomic-level perspective of epicathechin gallate fromJournal of biomolecular structure & dynamics · 2022Article
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- Pre-therapeutic efficacy of the CDK inhibitor dinaciclib in medulloblastoma cells.Scientific reports · 2021Article
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- Efficient apoptosis requires feedback amplification of upstream apoptotic signals by effector caspase-3 or -7.Science advances · 2019Article
- Gallic acid caused cultured mice TM4 Sertoli cells apoptosis and necrosis.Asian-Australasian journal of animal sciences · 2019Article
- The Apoptotic and Anti-apoptotic Effects of Pendimethalin and Trifluralin on A549 CellsTurkish journal of pharmaceutical sciences · 2018Article
- Effects of Remifentanil Preconditioning Attenuating Oxidative Stress in Human Dermal Fibroblast.Tissue engineering and regenerative medicine · 2017Article
- Propofol protects human keratinocytes from oxidative stress via autophagy expression.Journal of dental anesthesia and pain medicine · 2017Article
- A potential role of X-linked inhibitor of apoptosis protein in mitochondrial membrane permeabilization and its implication in cancer therapy.Drug discovery today · 2016Review
- Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy.PloS one · 2015Article
- Alpinetin inhibits lung cancer progression and elevates sensitization drug-resistant lung cancer cells to cis-diammined dichloridoplatium.Drug design, development and therapy · 2015Article
- Regulation of the intrinsic apoptosis pathway by reactive oxygen species.Antioxidants & redox signaling · 2013Review
- Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis.BMC cell biology · 2013Article
- Cleavage of anti-apoptotic Bcl-2 family members after TCR stimulation contributes to the decision between T cell activation and apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Promotion of Caspase Activation by Caspase-9-mediated Feedback Amplification of Mitochondrial Damage.Journal of clinical & cellular immunology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Proapoptotic Bcl-2 family members alter mitochondrial permeability resulting in the release of apoptogenic factors that initiate a caspase cascade. These changes are well described; however, the effects of caspases on mitochondrial function are less well characterized. Here we describe the consequence of caspase-9 and effector caspase inhibition on mitochondrial physiology during intrinsic cell death. Caspase inhibition prevents the complete loss of mitochondrial membrane potential without affecting cytochrome c release. When effector caspases are inhibited, mitochondria become uncoupled and produce reactive oxygen species. Interestingly, the effector caspase-mediated depolarization of the mitochondria occurs independent of the activity of complexes I-IV of the electron transport chain. In contrast, caspase-9 inhibition prevents mitochondrial uncoupling and ROS production and allows for continued electron transport despite the release of cytochrome c. Taken together, these data suggest that activated caspase-9 prevents the accessibility of cytochrome c to complex III, resulting in the production of reactive oxygen species, and that effector caspases may depolarize mitochondria to terminate ROS production and preserve an apoptotic phenotype.
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.