ArticlePloS one2014
Altered mitochondria morphology and cell metabolism in Apaf1-deficient cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Genome-Wide Association Study Reveals Novel Candidate Genes Influencing Semen Traits in Landrace Pigs.Animals : an open access journal from MDPI · 2024Article
- Jieduan-Niwan Formula Reduces Liver Apoptosis in a Rat Model of Acute-on-Chronic Liver Failure by Regulating the E2F1-Mediated Intrinsic Apoptosis Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Human Milk and Donkey Milk, Compared to Cow Milk, Reduce Inflammatory Mediators and Modulate Glucose and Lipid Metabolism, Acting on Mitochondrial Function and Oleylethanolamide Levels in Rat Skeletal Muscle.Frontiers in physiology · 2018Article
- Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway.Frontiers in neuroscience · 2018Article
- Intercellular mRNA trafficking via membrane nanotube-like extensions in mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Apaf1 inhibition promotes cell recovery from apoptosis.Protein & cell · 2015Article
- Apaf1-deficient cortical neurons exhibit defects in axonal outgrowth.Cellular and molecular life sciences : CMLS · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundApaf1 (apoptotic protease activating factor 1) is the central component of the apoptosome, a multiprotein complex that activates procaspase-9 after cytochrome c release from the mitochondria in the intrinsic pathway of apoptosis. Other cellular roles, including a pro-survival role, have also been described for Apaf1, while the relative contribution of each function to cell death, but also to cell homeostatic conditions, remain to be clarified. METHODOLOGY AND PRINCIPAL
findingsHere we examined the response to apoptosis induction of available embryonic fibroblasts from Apaf1 knockout mice (MEFS KO Apaf1). In the absence of Apaf1, cells showed mitochondria with an altered morphology that affects cytochrome c release and basal metabolic status.
conclusionsWe analysed mitochondrial features and cell death response to etoposide and ABT-737 in two different Apaf1-deficient MEFS, which differ in the immortalisation protocol. Unexpectedly, MEFS KO Apaf1 immortalised with the SV40 antigen (SV40IM-MEFS Apaf1) and those which spontaneously immortalised (SIM-MEFS Apaf1) respond differently to apoptotic stimuli, but both presented relevant differences at the mitochondria when compared to MEFS WT, indicating a role for Apaf1 at the mitochondria.
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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.