4.8 Article

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

Journal

NATURE GENETICS
Volume 42, Issue 2, Pages 170-U109

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/ng.512

Keywords

-

Funding

  1. NINDS
  2. Johns Hopkins Department of Neurology
  3. Elaine Potter Charitable Foundation
  4. NIH [R01GM081340]
  5. McKnight Scholar Award
  6. Medical Research Council [G0802760] Funding Source: researchfish
  7. MRC [G0802760] Funding Source: UKRI

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.8
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available