Evidence map›Paper›PMID 41973119›Full record

ArticleCellular and molecular neurobiology2026

MELK is Required for G2/M Phase Progression in Cortical Progenitors: Insights from Rare ASD-Associated Variants.

Liyang Zhao, Xianjing Li, Kang Yang, Miaomiao Jiang, Zhonghe Chen, Yiqian Shao, Tianlan Lu, Dai Zhang, Lifang Wang, Jun Li

Abstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Liyang Zhao *National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID http://orcid.org/0000-0002-5996-634X
Xianjing Li *National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0009-0007-8172-8499
Kang YangNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0009-0009-6394-327X
Miaomiao JiangNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0000-0003-1257-5373
Zhonghe ChenNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0009-0001-7350-9735
Yiqian ShaoNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0009-0002-5704-1842
Tianlan LuNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0009-0000-7839-4642
Dai ZhangNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-9162-7401
Lifang WangNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China. lifangwang@bjmu.edu.cn.ORCID https://orcid.org/0000-0003-0326-9235
Jun LiNational Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), NHC Key Laboratory of Mental Health (Peking University), Peking University Sixth Hospital, Peking University Institute of Mental Health, No. 51 Huayuanbei Road, Haidian District, Beijing, 100191, China. junli1985@bjmu.edu.cn.ORCID https://orcid.org/0000-0001-6448-8568

Funding

National Natural Science Foundation of China 82171537National Natural Science Foundation of China 82271576National Natural Science Foundation of China 82501856Non-profit Central Research Institute Chinese Academy of Medical Sciences 2023-PT320-08Postdoctoral Fellowship Program of CPSF GZC20251381the China Disabled Persons' Federation CDPF2023KF00001
6 · The paper itself

Abstract

Maternal embryonic leucine zipper kinase (MELK) is a cell cycle regulator, yet its role in embryonic cortical development remains unclear. We identified ultra-rare, predicted loss-of-function MELK variants in ASD individuals, prompting this functional investigation. Published human single-cell transcriptomics showed that MELK expression is enriched in neural progenitors and correlates with the G2/M phase. Using in utero electroporation in mouse cortex, we found that Melk knockdown reduced the proportion of progenitors in G2/M phase. Knockdown also caused impaired multipolar-to-bipolar transition and shorter leading processes. Complementing these findings, transcriptomic analysis of FACS-sorted Melk-knockdown cortical cells revealed downregulation of G2/M-related genes and cytoskeletal regulators linked to neuronal morphogenesis. Together, these findings identify MELK as a critical regulator of both G2/M phase progression and neuronal morphogenesis during cortical development, providing a mechanistic link to neurodevelopmental conditions.

Indexed as

Cell DivisionCerebral CortexG2 PhaseNeural Stem CellsProtein Serine-Threonine KinasesAnimalsGene Knockdown TechniquesHumansMiceNeurodevelopmentMELK protein, humanProtein Serine-Threonine KinasesCortical developmentG2/M phaseMELKNeuronal morphology

Identifiers

PMID41973119
PMCPMC13184066

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.