ArticleEMBO reports2014
A direct role of Mad1 in the spindle assembly checkpoint beyond Mad2 kinetochore recruitment.
Article in EMBO reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Loss of negative regulation by HDAC1 and REST contributes to MAD1 overexpression in breast cancer.Molecular biology of the cell · 2025Article
- Interplay of kinetochores and catalysts drives rapid assembly of the mitotic checkpoint complex.Nature communications · 2025Article
- Kinetochore-catalyzed MCC formation: A structural perspective.IUBMB life · 2023Article
- The structural flexibility of MAD1 facilitates the assembly of the Mitotic Checkpoint Complex.Nature communications · 2023Article
- Biallelic germline mutations in MAD1L1 induce a syndrome of aneuploidy with high tumor susceptibility.Science advances · 2022Article
- Aurora B phosphorylates Bub1 to promote spindle assembly checkpoint signaling.Current biology : CB · 2022Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Direct interactions of mitotic arrest deficient 1 (MAD1) domains with each other and MAD2 conformers are required for mitotic checkpoint signaling.The Journal of biological chemistry · 2018Article
- The closed form of Mad2 is bound to Mad1 and Cdc20 at unattached kinetochores.Cell cycle (Georgetown, Tex.) · 2018Article
- MAD1: Kinetochore Receptors and Catalytic Mechanisms.Frontiers in cell and developmental biology · 2018Review
- BubR1 Promotes Bub3-Dependent APC/C Inhibition during Spindle Assembly Checkpoint Signaling.Current biology : CB · 2017Article
- DNA damage induces a kinetochore-based ATM/ATR-independent SAC arrest unique to the first meiotic division in mouse oocytes.Development (Cambridge, England) · 2017Article
- Bub1 positions Mad1 close to KNL1 MELT repeats to promote checkpoint signalling.Nature communications · 2017Article
- Micromanaging checkpoint proteins.eLife · 2017Article
- A sequential multi-target Mps1 phosphorylation cascade promotes spindle checkpoint signaling.eLife · 2017Article
- Synthetic Physical Interactions Map Kinetochore-Checkpoint Activation Regions.G3 (Bethesda, Md.) · 2016Article
- TRIP13PCH-2 promotes Mad2 localization to unattached kinetochores in the spindle checkpoint response.The Journal of cell biology · 2015Article
- Distinct domains in Bub1 localize RZZ and BubR1 to kinetochores to regulate the checkpoint.Nature communications · 2015Article
- Signalling dynamics in the spindle checkpoint response.Nature reviews. Molecular cell biology · 2014Review
- Phosphorylation of nucleoporin Tpr governs its differential localization and is required for its mitotic function.Journal of cell science · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spindle assembly checkpoint (SAC) ensures accurate chromosome segregation by delaying entry into anaphase until all sister chromatids have become bi-oriented. A key component of the SAC is the Mad2 protein, which can adopt either an inactive open (O-Mad2) or active closed (C-Mad2) conformation. The conversion of O-Mad2 into C-Mad2 at unattached kinetochores is thought to be a key step in activating the SAC. The "template model" proposes that this is achieved by the recruitment of soluble O-Mad2 to C-Mad2 bound at kinetochores through its interaction with Mad1. Whether Mad1 has additional roles in the SAC beyond recruitment of C-Mad2 to kinetochores has not yet been addressed. Here, we show that Mad1 is required for mitotic arrest even when C-Mad2 is artificially recruited to kinetochores, indicating that it has indeed an additional function in promoting the checkpoint. The C-terminal globular domain of Mad1 and conserved residues in this region are required for this unexpected function of Mad1.
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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.