ArticleThe Journal of cell biology2010
Drosophila IAP antagonists form multimeric complexes to promote cell death.
Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 69 citations in OpenAlex.
- Hdac3 suppresses apoptosis through deacetylating and stabilizing the antiapoptotic protein Diap1.Science advances · 2026Article
- 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
- Chromosome-scale genome assembly of the South American fruit fly, Anastrepha fraterculus sp.1.Insect science · 2026Article
- Transcriptional repression of reaper by Stand still ensures female germline development in Drosophila.PLoS genetics · 2026Article
- A window of cell cycle plasticity enables imperfect regeneration of an adult postmitotic organ inbioRxiv : the preprint server for biology · 2025Article
- Understanding the molecular mechanism of regeneration through apoptosis-induced compensatory proliferation studies - updates and future aspects.Apoptosis : an international journal on programmed cell death · 2024Review
- A feedback loop that drives cell death and proliferation and its defect in intestinal stem cells.Life science alliance · 2024Article
- Article
- Keeping Cell Death Alive: An Introduction into the French Cell Death Research Network.Biomolecules · 2022Review
- Deep Conservation ofInsects · 2021Article
- The Hh pathway promotes cell apoptosis through Ci-Rdx-Diap1 axis.Cell death discovery · 2021Article
- A comprehensive in vivo screen for anti-apoptotic miRNAs indicates broad capacities for oncogenic synergy.Developmental biology · 2021Article
- Engorgement of Rhipicephalus haemaphysaloides ticks blocked by silencing a protein inhibitor of apoptosis.Experimental & applied acarology · 2021Article
- Methionine restriction breaks obligatory coupling of cell proliferation and death by an oncogene Src ineLife · 2021Article
- Effects on Dopaminergic Neurons Are Secondary in COX-Deficient Locomotor Dysfunction in Drosophila.iScience · 2020Article
- Pro-Apoptotic Function Analysis of the Reaper Homologue IBM1 inInternational journal of molecular sciences · 2020Article
- Natural Genetic Variation Screen inG3 (Bethesda, Md.) · 2019Article
- Molecular characterization of an inhibitor of apoptosis protein (Bioengineered · 2019Article
- I Spy in the Developing Fly a Multitude of Ways to Die.Journal of developmental biology · 2018Review
- Azadirachtin Affects the Growth ofFrontiers in physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptosis is a specific form of cell death that is important for normal development and tissue homeostasis. Caspases are critical executioners of apoptosis, and living cells prevent their inappropriate activation through inhibitor of apoptosis proteins (IAPs). In Drosophila, caspase activation depends on the IAP antagonists, Reaper (Rpr), Head involution defective (Hid), and Grim. These proteins share a common motif to bind Drosophila IAP1 (DIAP1) and have partially redundant functions. We now show that IAP antagonists physically interact with each other. Rpr is able to self-associate and also binds to Hid and Grim. We have defined the domain involved in self-association and demonstrate that it is critical for cell-killing activity in vivo. In addition, we show that Rpr requires Hid for recruitment to the mitochondrial membrane and for efficient induction of cell death in vivo. Both targeting of Rpr to mitochondria and forced dimerization strongly promotes apoptosis. Our results reveal the functional importance of a previously unrecognized multimeric IAP antagonist complex for the induction of apoptosis.
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What OpenQuestion holds
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.