ArticleCell reports2016
The X-Linked-Intellectual-Disability-Associated Ubiquitin Ligase Mid2 Interacts with Astrin and Regulates Astrin Levels to Promote Cell Division.
Article in Cell reports, 2016. 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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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
27 citing papers in PubMed.
- Bi-allelic variants in FSD1L cause a neurodevelopmental disorder overlapping with L1 syndrome.American journal of human genetics · 2026Article
- Aging activates escape of the silent X chromosome in the female mouse hippocampus.Science advances · 2025Article
- Ribosomal DNA arrays are the most H-DNA rich element in the human genome.NAR genomics and bioinformatics · 2025Article
- Human REXO4 is Required for Cell Cycle Progression.bioRxiv : the preprint server for biology · 2025Article
- TRIM Proteins and Antiviral Microtubule Reorganization: A Novel Component in Innate Immune Responses?Viruses · 2024Review
- Expanding the genetic and phenotypic spectrum of TRAPPC9 and MID2-related neurodevelopmental disabilities: report of two novel mutations, 3D-modelling, and molecular docking studies.Journal of human genetics · 2024Article
- An E3 ligase TRIM1 promotes colorectal cancer progression via K63-linked ubiquitination and activation of HIF1α.Oncogenesis · 2024Article
- Burden of Rare Copy Number Variants in Microcephaly: A Brazilian Cohort of 185 Microcephalic Patients and Review of the Literature.Journal of autism and developmental disorders · 2024Review
- Exploration of the ubiquitination-related molecular classification and signature to predict the survival and immune microenvironment in colon cancer.Frontiers in genetics · 2024Article
- The Molecular and Function Characterization of Porcine MID2.Animals : an open access journal from MDPI · 2023Article
- Opitz syndrome: improving clinical interpretation of intronic variants in MID1 gene.Pediatric research · 2023Article
- CCHCR1-astrin interaction promotes centriole duplication through recruitment of CEP72.BMC biology · 2022Article
- CLUH controls astrin-1 expression to couple mitochondrial metabolism to cell cycle progression.eLife · 2022Article
- CDK1-cyclin-B1-induced kindlin degradation drives focal adhesion disassembly at mitotic entry.Nature cell biology · 2022Article
- The E3 ligase TRIM1 ubiquitinates LRRK2 and controls its localization, degradation, and toxicity.The Journal of cell biology · 2022Article
- The myosin regulatory light chain Myl5 localizes to mitotic spindle poles and is required for proper cell division.Cytoskeleton (Hoboken, N.J.) · 2021Article
- Germline AGO2 mutations impair RNA interference and human neurological development.Nature communications · 2020Article
- Review
- Astrin: A Key Player in Mitosis and Cancer.Frontiers in cell and developmental biology · 2020Review
- Dissecting the mechanisms of cell division.The Journal of biological chemistry · 2019Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Mid1 and Mid2 are ubiquitin ligases that regulate microtubule dynamics and whose mutation is associated with X-linked developmental disorders. We show that astrin, a microtubule-organizing protein, co-purifies with Mid1 and Mid2, has an overlapping localization with Mid1 and Mid2 at intercellular bridge microtubules, is ubiquitinated by Mid2 on lysine 409, and is degraded during cytokinesis. Mid2 depletion led to astrin stabilization during cytokinesis, cytokinetic defects, multinucleated cells, and cell death. Similarly, expression of a K409A mutant astrin in astrin-depleted cells led to the accumulation of K409A on intercellular bridge microtubules and an increase in cytokinetic defects, multinucleated cells, and cell death. These results indicate that Mid2 regulates cell division through the ubiquitination of astrin on K409, which is critical for its degradation and proper cytokinesis. These results could help explain how mutation of MID2 leads to misregulation of microtubule organization and the downstream disease pathology associated with X-linked intellectual disabilities.
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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.