ArticleProceedings of the National Academy of Sciences of the United States of America2013
Caspase-dependent regulation of the ubiquitin-proteasome system through direct substrate targeting.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 19 citations in OpenAlex.
- AlphaFold3-based modeling uncovers the dynamic structural interface between full-length IAP antagonists and DIAP1 for apoptosis regulation in Drosophila.Cell communication and signaling : CCS · 2026Article
- E2 Ubiquitin-Conjugating Enzymes Regulates Dengue Virus-2 Replication inMicroorganisms · 2024Article
- Inhibition of TBL1 cleavage alleviates doxorubicin-induced cardiomyocytes death by regulating the Wnt/β-catenin signal pathway.Cardiovascular research · 2024Article
- Programmed cell death reshapes the central nervous system during metamorphosis in insects.Current opinion in insect science · 2021Review
- The Ubiquitin Conjugating Enzyme UbcD1 is Required for Notch Signaling Activation DuringFrontiers in genetics · 2021Article
- Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.PLoS pathogens · 2020Article
- Proapoptotic function of deubiquitinaseOncotarget · 2017Article
- Nuclear factor-κB-inducing kinase (NIK) contains an amino-terminal inhibitor of apoptosis (IAP)-binding motif (IBM) that potentiates NIK degradation by cellular IAP1 (c-IAP1).The Journal of biological chemistry · 2014Article
- Drosophila USP5 controls the activation of apoptosis and the Jun N-terminal kinase pathway during eye development.PloS one · 2014Article
- DrICE resurrects Grim to antagonize DIAP1.Cell cycle (Georgetown, Tex.) · 2014Article
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Abstract
Drosophila inhibitor of apoptosis (IAP) 1 (DIAP1) is an E3 ubiquitin ligase that regulates apoptosis in flies, in large part through direct inhibition and/or ubiquitinylation of caspases. IAP antagonists, such as Reaper, Hid, and Grim, are thought to induce cell death by displacing active caspases from baculovirus IAP repeat domains in DIAP1, but can themselves become targets of DIAP1-mediated ubiquitinylation. Herein, we demonstrate that Grim self-associates in cells and is ubiquitinylated by DIAP1 at Lys136 in an UbcD1-dependent manner, resulting in its rapid turnover. K48-linked ubiquitin chains are added almost exclusively to BIR2-bound Grim as a result of its structural proximity to DIAP1's RING domain. However, active caspases can simultaneously cleave Grim at Asp132, removing the lysine necessary for ubiquitinylation as well as any existing ubiquitin conjugates. Cleavage therefore enhances the stability of Grim and initiates a feed-forward caspase amplification loop, resulting in greater cell death. In summary, Grim is a caspase substrate whose cleavage promotes apoptosis by limiting, in a target-specific fashion, its ubiquitinylation and turnover by the proteasome.
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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.