Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain

Among the many genes linked to microcephaly primary hereditary (MCPH), mutations in the abnormal spindle-like microcephaly-associated (ASPM) gene are the most common cause (Bond et al., 2002;Ltard et al., 2018).ASPM is predominantly expressed in the progenitor cells of the developing brain, specifically in the ventricular and subventricular zones of the cerebral cortex, where its expression peaks during neurogenesis and declines postnatally (Bond et al., 2022).This developmentally regulated expression underscores its critical role in the expansion of the cerebral cortex.However, the pathological consequences of ASPM mutation in non-human primates remain unexplored.Given the lack of cerebral cortical gyrification in rodents as well as other small animals and the evolutionarily divergent functions of ASPM

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Journal
Protein & Cell
Published
2025-11-07
DOI
https://doi.org/10.1093/procel/pwaf097
Primary Topic
Microtubule and mitosis dynamics
Type
article
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article

Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain

Mingtian Pan, Liang Jiang, Shihua Li, Xiaojiang Li et al.
Protein & Cell
Microtubule and mitosis dynamics
article

Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain

Mingtian Pan, Liang Jiang, Shihua Li, Xiaojiang Li, Qianjin Guo, Peng Wu, Xiangyu Guo, Weili Yang, Fengwei Sun, Dajian He, Zhuchi Tu
article en

Abstract

Among the many genes linked to microcephaly primary hereditary (MCPH), mutations in the abnormal spindle-like microcephaly-associated (ASPM) gene are the most common cause (Bond et al., 2002;Ltard et al., 2018).ASPM is predominantly expressed in the progenitor cells of the developing brain, specifically in the ventricular and subventricular zones of the cerebral cortex, where its expression peaks during neurogenesis and declines postnatally (Bond et al., 2022).This developmentally regulated expression underscores its critical role in the expansion of the cerebral cortex.However, the pathological consequences of ASPM mutation in non-human primates remain unexplored.Given the lack of cerebral cortical gyrification in rodents as well as other small animals and the evolutionarily divergent functions of ASPM

Protein & Cell
Jinan University (CN), Shanghai Library (CN)
Openalex Percentile: Top 65%
Microtubule and mitosis dynamics
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Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain — Mingtian Pan, Liang Jiang, et al. · Protein & Cell (2025) | TGRS Research Map | TGRS