ArticleThe Journal of cell biology2004
Apaf-1 and caspase-9 accelerate apoptosis, but do not determine whether factor-deprived or drug-treated cells die.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 181 citations in OpenAlex.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Extracellular Vesicle Inhibitors Enhance Cholix-Induced Cell Death via Regulation of the JNK-Dependent Pathway.Toxins · 2024Article
- Dopaminergic neurons lacking Caspase-3 avoid apoptosis but undergo necrosis after MPTP treatment inducing a Galectin-3-dependent selective microglial phagocytic response.Cell death & disease · 2024Article
- A1 is induced by pathogen ligands to limit myeloid cell death and NLRP3 inflammasome activation.EMBO reports · 2023Article
- Nicotinamide Mononucleotide Adenylyl Transferase 2 Inhibition Aggravates Neurological Damage after Traumatic Brain Injury in a Rat Model.Journal of Korean Neurosurgical Society · 2023Article
- A cell transmembrane peptide chimeric M(27-39)-HTPP targeted therapy for hepatocellular carcinoma.iScience · 2023Article
- Mitochondrial DNA in cell death and inflammation.Biochemical Society transactions · 2023Review
- Mitochondrion-Mediated Cell Death through Erk1-Alox5 Independent of Caspase-9 Signaling.Cells · 2022Article
- Interferon-γ primes macrophages for pathogen ligand-induced killing via a caspase-8 and mitochondrial cell death pathway.Immunity · 2022Article
- Induction of apoptosis in A431 cells via ROS generation and p53-mediated pathway by chloroform fraction of Argemone mexicana (Pepaveraceae).Environmental science and pollution research international · 2022Article
- Upregulation of apoptotic protease activating factor-1 expression correlates with anti-tumor effect of taxane drug.Medical oncology (Northwood, London, England) · 2021Article
- Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021Review
- Onosma bracteata Wall. induces GEnvironmental science and pollution research international · 2021Article
- Mitochondria focused neurotherapeutics for spinal cord injury.Experimental neurology · 2020Review
- A small molecule interacts with VDAC2 to block mouse BAK-driven apoptosis.Nature chemical biology · 2019Article
- In the absence of apoptosis, myeloid cells arrest when deprived of growth factor, but remain viable by consuming extracellular glucose.Cell death and differentiation · 2019Article
- The Pyroptotic Cell Death Effector Gasdermin D Is Activated by Gout-Associated Uric Acid Crystals but Is Dispensable for Cell Death and IL-1β Release.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming.Cell stress · 2019Review
- Mitochondrial inner membrane permeabilisation enables mtDNA release during apoptosis.The EMBO journal · 2018Article
- Moxidectin inhibits glioma cell viability by inducing G0/G1 cell cycle arrest and apoptosis.Oncology reports · 2018Article
7 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
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis after growth factor withdrawal or drug treatment is associated with mitochondrial cytochrome c release and activation of Apaf-1 and caspase-9. To determine whether loss of Apaf-1, caspase-2, and caspase-9 prevented death of factor-starved cells, allowing them to proliferate when growth factor was returned, we generated IL-3-dependent myeloid lines from gene-deleted mice. Long after growth factor removal, cells lacking Apaf-1, caspase-9 or both caspase-9 and caspase-2 appeared healthy, retained intact plasma membranes, and did not expose phosphatidylserine. However, release of cytochrome c still occurred, and they failed to form clones when IL-3 was restored. Cells lacking caspase-2 alone had no survival advantage. Therefore, Apaf-1, caspase-2, and caspase-9 are not required for programmed cell death of factor-dependent cells, but merely affect its rate. In contrast, transfection with Bcl-2 provided long-term, clonogenic protection, and could act independently of the apoptosome. Unlike expression of Bcl-2, loss of Apaf-1, caspase-2, or caspase-9 would therefore be unlikely to enhance the survival of cancer cells.
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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.