ArticleThe Biochemical journal2007
Requirement of Apaf-1 for mitochondrial events and the cleavage or activation of all procaspases during genotoxic stress-induced apoptosis.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Role of Damage-Associated Molecular Patterns in Septic Acute Kidney Injury, From Injury to Recovery.Frontiers in immunology · 2021Review
- Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity.eLife · 2019Article
- Caspase-2 resides in the mitochondria and mediates apoptosis directly from the mitochondrial compartment.Cell death discovery · 2016Article
- Reduction of myeloid-derived suppressor cells and lymphoma growth by a natural triterpenoid.Journal of cellular biochemistry · 2015Article
- Article
- Apaf-1 inhibitors protect from unwanted cell death in in vivo models of kidney ischemia and chemotherapy induced ototoxicity.PloS one · 2014Article
- HOXB1 restored expression promotes apoptosis and differentiation in the HL60 leukemic cell line.Cancer cell international · 2013Article
- Inhibition of Cell Growth and Induction of Apoptosis by Antrodia camphorata in HER-2/neu-Overexpressing Breast Cancer Cells through the Induction of ROS, Depletion of HER-2/neu, and Disruption of the PI3K/Akt Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Different signaling pathways stimulate a disintegrin and metalloprotease-17 (ADAM17) in neutrophils during apoptosis and activation.The Journal of biological chemistry · 2011Article
- Activation of caspase-9, but not caspase-2 or caspase-8, is essential for heat-induced apoptosis in Jurkat cells.The Journal of biological chemistry · 2010Article
- The role of caspase-2 in stress-induced apoptosis.Journal of cellular and molecular medicine · 2010Review
- KU135, a novel novobiocin-derived C-terminal inhibitor of the 90-kDa heat shock protein, exerts potent antiproliferative effects in human leukemic cells.Molecular pharmacology · 2009Article
- Caspase-9 activation by the apoptosome is not required for fas-mediated apoptosis in type II Jurkat cells.The Journal of biological chemistry · 2009Article
- A nanoconjugate Apaf-1 inhibitor protects mesothelial cells from cytokine-induced injury.PloS one · 2009Article
- Cleavage of Bid by executioner caspases mediates feed forward amplification of mitochondrial outer membrane permeabilization during genotoxic stress-induced apoptosis in Jurkat cells.The Journal of biological chemistry · 2009Article
- Caspase-mediated Bak activation and cytochrome c release during intrinsic apoptotic cell death in Jurkat cells.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Sequential activation of caspases is critical for the execution of apoptosis. Recent evidence suggests caspase 2 is a significant upstream caspase capable of initiating mitochondrial events, such as the release of cytochrome c. In particular, in vitro studies using recombinant proteins have shown that cleaved caspase 2 can induce mitochondrial outer membrane permeabilization directly or by cleaving the BH3-only protein BID (BH3 interacting domain death agonist). However, whether interchain cleavage or activation of procaspase 2 occurs prior to Apaf-1-mediated procaspase 9 activation under more natural conditions remains unresolved. In the present study, we show that Apaf-1-deficient Jurkat T-lymphocytes and mouse embryonic fibroblasts were highly resistant to DNA-damage-induced apoptosis and failed to cleave or activate any apoptotic procaspase, including caspase 2. Significantly, drug-induced cytochrome c release and loss of mitochondrial membrane potential were inhibited in cells lacking Apaf-1. By comparison, procaspase proteolysis and apoptosis were only delayed slightly in Apaf-1-deficient Jurkat cells upon treatment with anti-Fas antibody. Our data support a model in which Apaf-1 is necessary for the cleavage or activation of all procaspases and the promotion of mitochondrial apoptotic events induced by genotoxic drugs.
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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.