Evidence map›Paper›PMID 30765517›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Opposite regulation of Wnt/β-catenin and Shh signaling pathways by Rack1 controls mammalian cerebellar development.

Haihong Yang, Qian Zhu, Juanxian Cheng, Yan Wu, Ming Fan, Jiyan Zhang, Haitao Wu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  6. Atypical Cadherin FAT2 Is Required for Synaptic Integrity and Motor Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  9. CBX2 suppresses interferon signaling to diminish tumor immunogenicity via a noncanonical corepressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  16. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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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

7 authors at 1 institution in 1 country.

Haihong YangDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.ORCID 0000-0002-9618-1859
Qian ZhuDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.
Juanxian ChengDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.
Yan WuDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.
Ming FanDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.
Jiyan ZhangDepartment of Neuroimmunology and Antibody Engineering, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China zhangjy@nic.bmi.ac.cn wuht@bmi.ac.cn.
Haitao WuDepartment of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China; zhangjy@nic.bmi.ac.cn wuht@bmi.ac.cn.ORCID 0000-0001-8437-3194
Beijing Institute of Education · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of the cerebellum depends on intricate processes of neurogenesis, migration, and differentiation of neural stem cells (NSCs) and progenitor cells. Defective cerebellar development often results in motor dysfunctions and psychiatric disorders. Understanding the molecular mechanisms that underlie the complex development of the cerebellum will facilitate the development of novel treatment options. Here, we report that the receptor for activated C kinase (Rack1), a multifaceted signaling adaptor protein, regulates mammalian cerebellar development in a cell type-specific manner. Selective deletion of Rack1 in mouse NSCs or granule neuron progenitors (GNPs), but not Bergmann glial cells (BGs), causes severe defects in cerebellar morphogenesis, including impaired folia and fissure formation. NSCs and GNPs lacking Rack1 exhibit enhanced Wnt/β-catenin signaling but reduced Sonic hedgehog (Shh) signaling. Simultaneous deletion of β-catenin in NSCs, but not GNPs, significantly rescues the

Indexed as

Animalsbeta CateninCerebellumGene Expression Regulation, DevelopmentalHedgehog ProteinsHistone Deacetylase 1Histone Deacetylase 2MiceMice, KnockoutNeural Stem CellsNeuronsReceptors for Activated C KinaseSignal TransductionWnt Proteinsbeta CateninHdac1 protein, mouseHdac2 protein, mouseHedgehog ProteinsHistone Deacetylase 1Histone Deacetylase 2RACK1 protein, mouseReceptors for Activated C KinaseShh protein, mouseWnt Proteinscerebellar morphogenesisgranule neuron progenitorsHDAC1/HDAC2neural stem cellsRack1

Identifiers

PMID30765517
PMCPMC6410857
OpenAlexW2913269951

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.