ArticleMolecular cell2013
Mitosis-specific regulation of nuclear transport by the spindle assembly checkpoint protein Mad1p.
Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- Ulp1 association with nuclear pore complexes is required for the maintenance of global SUMOylation.Molecular biology of the cell · 2025Article
- Phosphorylation of Mad1 at serine 18 by Mps1 is required for the full virulence of rice blast fungus, Magnaporthe oryzae.Molecular plant pathology · 2024Article
- Phosphorylation-dependent mitotic SUMOylation drives nuclear envelope-chromatin interactions.The Journal of cell biology · 2021Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Multifunctionality of F-rich nucleoporins.Biochemical Society transactions · 2020Review
- Cyclin B1-Cdk1 facilitates MAD1 release from the nuclear pore to ensure a robust spindle checkpoint.The Journal of cell biology · 2020Article
- Effectors of the spindle assembly checkpoint are confined within the nucleus of Saccharomyces cerevisiae.Biology open · 2019Article
- Mad1 destabilizes p53 by preventing PML from sequestering MDM2.Nature communications · 2019Article
- Article
- Identification of the NovelG3 (Bethesda, Md.) · 2018Article
- A Mad2-Mediated Translational Regulatory Mechanism Promoting S-Phase Cyclin Synthesis Controls Origin Firing and Survival to Replication Stress.Molecular cell · 2018Article
- A novel function for the mitotic checkpoint protein Mad2p in translation.Molecular & cellular oncology · 2018Article
- Article
- Living in CIN: Mitotic Infidelity and Its Consequences for Tumor Promotion and Suppression.Developmental cell · 2016Review
- Synthetic Physical Interactions Map Kinetochore-Checkpoint Activation Regions.G3 (Bethesda, Md.) · 2016Article
- The spindle assembly checkpoint promotes chromosome bi-orientation: A novel Mad1 role in chromosome alignment.Cell cycle (Georgetown, Tex.) · 2016Review
- Review
- Control of the spindle checkpoint by lateral kinetochore attachment and limited Mad1 recruitment.Molecular biology of the cell · 2015Article
- Aneuploidy and chromosomal instability in cancer: a jackpot to chaos.Cell division · 2015Article
- A Golgi-localized pool of the mitotic checkpoint component Mad1 controls integrin secretion and cell migration.Current biology : CB · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear pore complexes (NPCs) and kinetochores perform distinct tasks, yet their shared ability to bind several proteins suggests their functions are intertwined. Among these shared proteins is Mad1p, a component of the yeast spindle assembly checkpoint (SAC). Here we describe a role for Mad1p in regulating nuclear import that employs its ability to sense a disruption of kinetochore-microtubule interactions during mitosis. We show that kinetochore-microtubule detachment arrests nuclear import mediated by the transport factor Kap121p through a mechanism that requires Mad1p cycling between unattached, metaphase kinetochores and binding sites at the NPC. This signaling pathway requires the Aurora B-like kinase Ipl1p, and the resulting transport changes inhibit the nuclear import of Glc7p, a phosphatase that acts as an Ipl1p antagonist. We propose that a distinct branch of the SAC exists in which Mad1p senses unattached kinetochores and, by altering NPC transport activity, regulates the nuclear environment of the spindle.
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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.