Evidence map›Paper›PMID 30021166›Full record

ArticleCell reports2018

Neuron-Specific Menin Deletion Leads to Synaptic Dysfunction and Cognitive Impairment by Modulating p35 Expression.

Kai Zhuang, Changquan Huang, Lige Leng, Honghua Zheng, Yuehong Gao, Guimiao Chen, Zhilin Ji, Hao Sun, Yu Hu, Di Wu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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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

19 authors at 2 institutions in 2 countries.

Kai ZhuangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Changquan HuangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Lige LengFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Honghua ZhengFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Yuehong GaoFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Guimiao ChenFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Zhilin JiFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Hao SunFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Yu HuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Di WuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Meng ShiFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Huifang LiFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Yingjun ZhaoFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China; Neuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Yunwu ZhangNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Maoqiang XueDepartment of Basic Medical Science, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Guojun BuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China; Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Timothy Y HuangNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Huaxi XuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China; Neuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Jie ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, Fujian 361102, China. Electronic address: jiezhang@xmu.edu.cn.
Xiamen University · CNDiscovery Institute · US

Funding

Molecular pathobiology of soluble TREM2 in Alzheimer's disease.RF1AG056130 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI, ZHAO, NA · 2017 to 2023
$6.8M
Regulation of Protein Trafficking in NeurodegenerationR01NS046673 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2003 to 2018
$5.8M
BAC Transgenic Mouse Models of TREM2 to Study Neuroprotective Mechanisms in ADRF1AG056114 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2017 to 2017
$4.1M
The Role of Appoptosin in Alzheimer's Disease and Other TauopathiesR01AG038710 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2011 to 2019
$3.9M
Identifying genes in Beta-Amyloid ProductionR01AG021173 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2004 to 2015
$3.3M
Characterizing neuroprotective roles for SNX27 signaling pathways in AD and DSRF1AG044420 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI · 2018 to 2018
$2.4M
Roles of SN27 in regulating glutamate receptors during neurodegenerationR01AG044420 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2013 to 2017
$2.0M
A role for TREM2/Abeta interactions in microglia-regulated AD pathogenesisR21AG059217 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI · 2018 to 2019
$536k
The Role of DLG5 in Alzheimer's DiseaseR21AG048519 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2015 to 2016
$536k
NIA NIH HHS R01 AG021173NIA NIH HHS R01 AG038710NIA NIH HHS R01 AG044420NIA NIH HHS R21 AG048519NIA NIH HHS R21 AG059217NIA NIH HHS RF1 AG044420NIA NIH HHS RF1 AG056114NIA NIH HHS RF1 AG056130NINDS NIH HHS R01 NS046673
6 · The paper itself

Abstract

Menin (MEN1) is a critical modulator of tissue development and maintenance. As such, MEN1 mutations are associated with multiple endocrine neoplasia type 1 (MEN1) syndrome. Although menin is abundantly expressed in the nervous system, little is known with regard to its function in the adult brain. Here, we demonstrate that neuron-specific deletion of Men1 (CcKO) affects dendritic branching and spine formation, resulting in defects in synaptic function, learning, and memory. Furthermore, we find that menin binds to the p35 promoter region to facilitate p35 transcription. As a primary Cdk5 activator, p35 is expressed mainly in neurons and is critical for brain development and synaptic plasticity. Restoration of p35 expression in the hippocampus and cortex of Men1 CcKO mice rescues synaptic and cognitive deficits associated with Men1 deletion. These results reveal a critical role for menin in synaptic and cognitive function by modulating the p35-Cdk5 pathway.

Indexed as

AnimalsCognitive DysfunctionGene Expression RegulationGenetic LociMemory DisordersMice, KnockoutNeuronsOrgan SpecificityPhosphotransferasesPromoter Regions, GeneticProto-Oncogene ProteinsSynapsesTranscription, GeneticCdk5r1 protein, mouseMen1 protein, mousePhosphotransferasesProto-Oncogene ProteinsCdk5cognitionmeninp35synaptic function

Identifiers

PMID30021166
PMCPMC6434950
OpenAlexW2883901424

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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.