Compound heterozygous mutations of NTNG2 cause intellectual disability via inhibition of the CaMKII signaling-Reference-Cited by-同舟云学术

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Compound heterozygous mutations of NTNG2 cause intellectual disability via inhibition of the CaMKII signaling

Published:2024-08 Issue: Volume: Page:
ISSN:1673-8527
Container-title:Journal of Genetics and Genomics
language:en
Short-container-title:Journal of Genetics and Genomics

Author:

Chen Yaoting,Chen Jiang,Liang Lili,Dai Weiqian,Li Nan,Dong Shuangshuang,Zhan Yongkun,Chen Guiquan,Yu Yongguo^ORCID

Funder

National Natural Science Foundation of China-Yunnan Joint Fund

National Aerospace Science Foundation of China

Shanghai Jiaotong University

Science and Technology Commission of Fengxian District, Shanghai Municipality

Scientific and Innovative Action Plan of Shanghai

National Key Clinical Specialty Discipline Construction Program of China

Publisher

Elsevier BV

Reference42 articles.

1. Homozygous frameshift variant in NTNG2, encoding a synaptic cell adhesion molecule, in individuals with developmental delay, hypotonia, and autistic features;Abu-Libdeh;Neurogenetics,2019

2. Impairment of spatial but not contextual memory in CaMKII mutant mice with a selective loss of hippocampal LTP in the range of the theta frequency;Bach;Cell,1995

3. Control of GluR1 AMPA receptor function by cAMP-dependent protein kinase;Banke;J. Neurosci.,2000

4. Identification of the Ca2+/calmodulin-dependent protein kinase II regulatory phosphorylation site in the alpha-amino-3-hydroxyl-5-methyl-4- isoxazole-propionate-type glutamate receptor;Barria;J. Biol. Chem.,1997

5. Synaptophysin chaperones the assembly of 12 SNAREpins under each ready-release vesicle;Bera;Proc. Natl. Acad. Sci. U. S. A.,2023

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