ArticleThe Journal of biological chemistry2009
Cleavage of Bid by executioner caspases mediates feed forward amplification of mitochondrial outer membrane permeabilization during genotoxic stress-induced apoptosis in Jurkat cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Bid Protein: A Participant in the Apoptotic Network with Roles in Viral Infections.International journal of molecular sciences · 2025Review
- Glucose limitation protects cancer cells from apoptosis induced by pyrimidine restriction and replication inhibition.Nature metabolism · 2024Article
- Radiotherapy-Induced Neurocognitive Impairment Is Driven by Heightened Apoptotic Priming in Early Life and Prevented by Blocking BAX.Cancer research · 2023Article
- Sidestream Smoke Extracts from Harm-Reduction and Conventional Camel Cigarettes Inhibit Osteogenic Differentiation via Oxidative Stress and Differential Activation of intrinsic Apoptotic Pathways.Antioxidants (Basel, Switzerland) · 2022Article
- Landfill soil leachates from Nigeria and India induced DNA damage and alterations in genes associated with apoptosis in Jurkat cell.Environmental science and pollution research international · 2022Article
- An AMPK-caspase-6 axis controls liver damage in nonalcoholic steatohepatitis.Science (New York, N.Y.) · 2020Article
- Article
- Tumor suppressor BLU promotes TRAIL-induced apoptosis by downregulating NF-κB signaling in nasopharyngeal carcinoma.Oncotarget · 2017Article
- Farnesylthiosalicylic acid sensitizes hepatocarcinoma cells to artemisinin derivatives.PloS one · 2017Article
- Caspase-cleaved arrestin-2 and BID cooperatively facilitate cytochrome C release and cell death.Cell death and differentiation · 2014Article
- The progression of cell death affects the rejection of allogeneic tumors in immune-competent mice - implications for cancer therapy.Frontiers in immunology · 2014Article
- Induction of Cell Death Mechanisms and Apoptosis by Nanosecond Pulsed Electric Fields (nsPEFs).Cells · 2013Article
- Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies.British journal of pharmacology · 2012Review
- Apoptosis induction of U937 human leukemia cells by diallyl trisulfide induces through generation of reactive oxygen species.Journal of biomedical science · 2012Article
- BID is a critical factor controlling cell viability regulated by IFN-α.Journal of immunotherapy (Hagerstown, Md. : 1997) · 2012Article
- Different signaling pathways stimulate a disintegrin and metalloprotease-17 (ADAM17) in neutrophils during apoptosis and activation.The Journal of biological chemistry · 2011Article
- Article
- A suicide gene approach using the human pro-apoptotic protein tBid inhibits HIV-1 replication.BMC biotechnology · 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
- TRAIL-activated stress kinases suppress apoptosis through transcriptional upregulation of MCL-1.Cell death and differentiation · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The extent to which the BH3-only protein Bid is important for intrinsic (mitochondria-mediated) apoptotic cell death induced by genotoxic stress remains controversial. In the present study, we examine this issue using a panel of gene-manipulated Bax-deficient Jurkat T-lymphocytes. Cells stably depleted of Bid were far less sensitive than control-transfected cells to etoposide-induced apoptosis. In particular, drug-induced Bak activation, cytochrome c release, loss of mitochondrial membrane potential, and caspase activation were all decreased in cells lacking Bid. Reconstitution experiments using recombinant proteins and permeabilized Bid-deficient cells demonstrated that truncated Bid (tBid), but not full-length Bid, potently induced Bak activation and the release of cytochrome c. Further, caspase-8-deficient Jurkat cells efficiently cleaved Bid and were sensitive to drug-induced apoptosis. By comparison, Apaf-1-deficient cells, as well as cells overexpressing full-length X-linked inhibitor of apoptosis protein (XIAP) or the BIR1/BIR2 domains of XIAP, failed to cleave Bid in response to genotoxic stress. These data suggest that tBid plays an important regulatory role in the execution of DNA damage-induced cytochrome c release and apoptosis. However, the fact that cleavage of Bid to tBid is mediated by executioner caspases suggests that a self-amplifying feed forward loop involving caspases, Bid, and mitochondria may help determine irreversible commitment to apoptosis.
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