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TRPV4 基因突变导致 2C 型腓骨肌萎缩症。

Mutations in TRPV4 cause Charcot-Marie-Tooth disease type 2C.

机构信息

Department of Medicine, University College London, UK.

出版信息

Nat Genet. 2010 Feb;42(2):170-4. doi: 10.1038/ng.512. Epub 2009 Dec 27.


DOI:10.1038/ng.512
PMID:20037586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2812627/
Abstract

Charcot-Marie-Tooth disease type 2C (CMT2C) is an autosomal dominant neuropathy characterized by limb, diaphragm and laryngeal muscle weakness. Two unrelated families with CMT2C showed significant linkage to chromosome 12q24.11. We sequenced all genes in this region and identified two heterozygous missense mutations in the TRPV4 gene, C805T and G806A, resulting in the amino acid substitutions R269C and R269H. TRPV4 is a well-known member of the TRP superfamily of cation channels. In TRPV4-transfected cells, the CMT2C mutations caused marked cellular toxicity and increased constitutive and activated channel currents. Mutations in TRPV4 were previously associated with skeletal dysplasias. Our findings indicate that TRPV4 mutations can also cause a degenerative disorder of the peripheral nerves. The CMT2C-associated mutations lie in a distinct region of the TRPV4 ankyrin repeats, suggesting that this phenotypic variability may be due to differential effects on regulatory protein-protein interactions.

摘要

腓骨肌萎缩症 2C 型(CMT2C)是一种常染色体显性遗传性周围神经病,其特征是肢体、膈肌和喉肌无力。两个不相关的 CMT2C 家系与染色体 12q24.11 存在显著连锁。我们对该区域的所有基因进行了测序,在 TRPV4 基因中发现了两个杂合错义突变 C805T 和 G806A,导致氨基酸取代 R269C 和 R269H。TRPV4 是 TRP 阳离子通道超家族的知名成员。在 TRPV4 转染细胞中,CMT2C 突变导致明显的细胞毒性和增加的组成型和激活的通道电流。TRPV4 突变先前与骨骼发育不良有关。我们的研究结果表明,TRPV4 突变也可引起周围神经的退行性疾病。与 CMT2C 相关的突变位于 TRPV4 锚蛋白重复的一个独特区域,表明这种表型变异性可能是由于对调节蛋白-蛋白相互作用的不同影响所致。

相似文献

[1]
Mutations in TRPV4 cause Charcot-Marie-Tooth disease type 2C.

Nat Genet. 2009-12-27

[2]
Scapuloperoneal spinal muscular atrophy and CMT2C are allelic disorders caused by alterations in TRPV4.

Nat Genet. 2009-12-27

[3]
Incidence and Clinical Features of TRPV4-Linked Axonal Neuropathies in a USA Cohort of Charcot-Marie-Tooth Disease Type 2.

Neuromolecular Med. 2020-3

[4]
TRPV4 mutations and cytotoxic hypercalcemia in axonal Charcot-Marie-Tooth neuropathies.

Neurology. 2011-2-2

[5]
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Neurology. 2010-11-30

[6]
Alterations in the ankyrin domain of TRPV4 cause congenital distal SMA, scapuloperoneal SMA and HMSN2C.

Nat Genet. 2009-12-27

[7]
TRPV4 neuromuscular disease registry highlights bulbar, skeletal and proximal limb manifestations.

Brain. 2025-1-7

[8]
Channelopathies converge on TRPV4.

Nat Genet. 2010-2

[9]
A TRPV4 mutation caused Charcot-Marie-Tooth disease type 2C with scapuloperoneal muscular atrophy overlap syndrome and scapuloperoneal spinal muscular atrophy in one family: a case report and literature review.

BMC Neurol. 2023-6-30

[10]
Phenotypic variability of TRPV4 related neuropathies.

Neuromuscul Disord. 2015-6

引用本文的文献

[1]
A QUARTER CENTURY OF CALCIUM-PERMEABLE ION CHANNEL, TRPV4: PERSPECTIVES ON EXPRESSION AND FUNCTION IN ENDOTHELIAL CELLS-TIME TO TRANSLATE.

Trans Am Clin Climatol Assoc. 2025

[2]
Rare Variants Cause Charcot-Marie-Tooth Disease in Malian Families.

Brain Behav. 2025-5

[3]
Delineating the genetic landscape of Charcot-Marie-tooth disease in Türkiye: Distinct distribution, rare phenotypes, and novel variants.

Eur J Neurol. 2025-1

[4]
TRPV4 activation by core body temperature has multimodal functions in the central nervous system.

J Physiol Sci. 2024-11-22

[5]
Clinical and Genetic Profiles of 5q- and Non-5q-Spinal Muscular Atrophy Diseases in Pediatric Patients.

Genes (Basel). 2024-9-30

[6]
Combined clinical, structural and cellular studies discriminate pathogenic and benign TRPV4 variants.

Brain. 2025-2-3

[7]
Identification and Properties of TRPV4 Mutant Channels Present in Polycystic Kidney Disease Patients.

Function (Oxf). 2024-9-10

[8]
Clinical Characteristics and Whole Exome Sequencing Analysis in Serbian Cases of Clubfoot Deformity-Single Center Study.

Children (Basel). 2024-5-27

[9]
TRPV4 neuromuscular disease registry highlights bulbar, skeletal and proximal limb manifestations.

Brain. 2025-1-7

[10]
Gain-of-function mutations of TRPV4 acting in endothelial cells drive blood-CNS barrier breakdown and motor neuron degeneration in mice.

Sci Transl Med. 2024-5-22

本文引用的文献

[1]
Differential regulation of TRPV1, TRPV3, and TRPV4 sensitivity through a conserved binding site on the ankyrin repeat domain.

J Biol Chem. 2009-10-28

[2]
The vanilloid transient receptor potential channel TRPV4: from structure to disease.

Prog Biophys Mol Biol. 2009-10-14

[3]
Identification and characterization of novel TRPV4 modulators.

Biochem Biophys Res Commun. 2009-11-20

[4]
A point mutation in TRPC3 causes abnormal Purkinje cell development and cerebellar ataxia in moonwalker mice.

Proc Natl Acad Sci U S A. 2009-4-21

[5]
Mutations in the gene encoding the calcium-permeable ion channel TRPV4 produce spondylometaphyseal dysplasia, Kozlowski type and metatropic dysplasia.

Am J Hum Genet. 2009-3

[6]
Molecular mechanisms of TRPV4-mediated neural signaling.

Ann N Y Acad Sci. 2008-11

[7]
Motor deficit in a Drosophila model of mucolipidosis type IV due to defective clearance of apoptotic cells.

Cell. 2008-11-28

[8]
Gain-of-function mutations in TRPV4 cause autosomal dominant brachyolmia.

Nat Genet. 2008-8

[9]
Interplay between TRP channels and the cytoskeleton in health and disease.

Eur J Cell Biol. 2008-9

[10]
Structural analyses of the ankyrin repeat domain of TRPV6 and related TRPV ion channels.

Biochemistry. 2008-2-26

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