ReviewMolecular neurobiology2018
The Role of WD40-Repeat Protein 62 (MCPH2) in Brain Growth: Diverse Molecular and Cellular Mechanisms Required for Cortical Development.
Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Prenatal Diagnosis of Autosomal Recessive Primary Microcephaly Type 2 Caused by Compound Heterozygous WDR62 Variants in a Family With Two Recurrent Cases.Molecular genetics & genomic medicine · 2026Article
- A Human Neural Tube Model Using 4D Self-Folding Smart Scaffolds.Advanced healthcare materials · 2026Article
- WDR62 is required for proper proliferation and early differentiation of skeletal myoblasts.Communications biology · 2026Article
- Autosomal recessive primary microcephaly type 2 associated with a novelFrontiers in neurology · 2024Article
- Article
- WDR62 variants contribute to congenital heart disease by inhibiting cardiomyocyte proliferation.Clinical and translational medicine · 2022Article
- Proximity labeling reveals non-centrosomal microtubule-organizing center components required for microtubule growth and localization.Current biology : CB · 2021Article
- WDR62 regulates spindle dynamics as an adaptor protein between TPX2/Aurora A and katanin.The Journal of cell biology · 2021Article
- A Novel Homozygous Frameshift WDR81 Mutation associated with Microlissencephaly, Corpus Callosum Agenesis, and Pontocerebellar Hypoplasia.Journal of pediatric genetics · 2021Article
- Pathophysiological Significance of WDR62 and JNK Signaling in Human Diseases.Frontiers in cell and developmental biology · 2021Review
- Review
- The Spindle-Associated Microcephaly Protein, WDR62, Is Required for Neurogenesis and Development of the Hippocampus.Frontiers in cell and developmental biology · 2020Article
- Review
- Mutations in the microtubule-associated protein MAP11 (C7orf43) cause microcephaly in humans and zebrafish.Brain : a journal of neurology · 2019Article
- MEKK3 coordinates with FBW7 to regulate WDR62 stability and neurogenesis.PLoS biology · 2018Article
- A novel non sense mutation in WDR62 causes autosomal recessive primary microcephaly: a case report.BMC medical genetics · 2018Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Genetic disruptions of spindle/centrosome-associated WD40-repeat protein 62 (WDR62) are causative for autosomal recessive primary microcephaly (MCPH) and a broader range of cortical malformations. Since the identification of WDR62 as encoded by the MCPH2 locus in 2010, recent studies that have deleted/depleted WDR62 in various animal models of cortical development have highlighted conserved functions in brain growth. Here, we provide a timely review of our current understanding of WDR62 contributions in the self-renewal, expansion and fate specification of neural stem and progenitor cells that are critical for neocortical development. Recent studies have revealed multiple functions for WDR62 in the regulation of spindle organization, mitotic progression and the duplication and biased inheritance of centrosomes during asymmetric divisions. We also discuss recently elaborated WDR62 interaction partners that include Aurora and c-Jun N-terminal kinases as part of complex signalling mechanisms that may define its neural functions. These studies provide new insights into the molecular and cellular processes that are required for brain formation and implicated in the genesis of primary microcephaly.
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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.