ArticleMolecular cell2015
An Inhibitor of PIDDosome Formation.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 40 citations in OpenAlex.
- PARP4 ADP-ribosylates PIDD1 to complete a phospho/SUMO/PAR-ylation cascade that orchestrates PIDDosome assembly.Science advances · 2026Article
- High-throughput screening identifies a previously undescribed checkpoint controlling mitotic progression in response to DNA damage.The FEBS journal · 2025Article
- Stepwise phosphorylation and SUMOylation of PIDD1 drive PIDDosome assembly in response to DNA repair failure.Nature communications · 2024Article
- PIDD1 in cell cycle control, sterile inflammation and cell death.Biochemical Society transactions · 2022Review
- Increased BUB1B/BUBR1 expression contributes to aberrant DNA repair activity leading to resistance to DNA-damaging agents.Oncogene · 2021Article
- FANCI functions as a repair/apoptosis switch in response to DNA crosslinks.Developmental cell · 2021Article
- The p53-caspase-2 axis in the cell cycle and DNA damage response.Experimental & molecular medicine · 2021Review
- A Switch in p53 Dynamics Marks Cells That Escape from DSB-Induced Cell Cycle Arrest.Cell reports · 2020Article
- Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020Review
- How Cells Handle DNA Breaks during Mitosis: Detection, Signaling, Repair, and Fate Choice.Cells · 2019Review
- Human cytomegalovirus glycoprotein B variants affect viral entry, cell fusion, and genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A role for caspase-2 in sphingosine kinase 1 proteolysis in response to doxorubicin in breast cancer cells - implications for the CHK1-suppressed pathway.FEBS open bio · 2018Article
- NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus.The Journal of cell biology · 2017Article
- Direct pro-apoptotic role for NPM1 as a regulator of PIDDosome formation.Molecular & cellular oncology · 2017Article
- Caspase 2 in mitotic catastrophe: The terminator of aneuploid and tetraploid cells.Molecular & cellular oncology · 2017Article
- A mitosis-sensing caspase activation platform? New insights into the PIDDosome.Molecular & cellular oncology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The PIDDosome-PIDD-RAIDD-caspase-2 complex-is a proapoptotic caspase-activation platform of elusive significance. DNA damage can initiate complex assembly via ATM phosphorylation of the PIDD death domain (DD), which enables RAIDD recruitment to PIDD. In contrast, the mechanisms limiting PIDDosome formation have remained unclear. We identify the mitotic checkpoint factor BubR1 as a direct PIDDosome inhibitor, acting in a noncanonical role independent of Mad2. Following its phosphorylation by ATM at DNA breaks, "primed" PIDD relocates to kinetochores via a direct interaction with BubR1. BubR1 binds the PIDD DD, competes with RAIDD recruitment, and negates PIDDosome-mediated apoptosis after ionizing radiation. The PIDDosome thus sequentially integrates DNA damage and mitotic checkpoint signals to decide cell fate in response to genotoxic stress. We further show that by sequestering PIDD at the kinetochore, BubR1 acts to delay PIDDosome formation until the next cycle, defining a new mechanism by which cells evade apoptosis during mitosis.
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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.