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Genetic inactivation of Trpml3 does not lead to hearing and vestibular impairment in mice.

TRPML3, a member of the transient receptor potential (TRP) family, is an inwardly rectifying, non-selective Ca2+-permeable cation channel that is regulated by extracytosolic Na+ and H+ and can be activated by a variety of small molecules. The severe auditory and vestibular phenotype of the TRPML3(A419P) varitint-waddler mutation made this protein particularly interesting for inner ear biology. To elucidate the physiological role of murine TRPML3, we conditionally inactivated Trpml3 in mice. Surprisingly, lack of functional TRPML3 did not lead to circling behavior, balance impairment or hearing loss.

Pubmed ID: 21179200


  • Jörs S
  • Grimm C
  • Becker L
  • Heller S


PloS one

Publication Data

December 23, 2010

Associated Grants

  • Agency: NIDCD NIH HHS, Id: DC004563
  • Agency: NIDCD NIH HHS, Id: P30 DC010363
  • Agency: NIDCD NIH HHS, Id: R01 DC004563

Mesh Terms

  • Animals
  • Brain Stem
  • Cations
  • Cell Line
  • Cytosol
  • Exons
  • Gene Deletion
  • Genotype
  • Hearing
  • Hearing Loss
  • Humans
  • Hydrogen
  • Mice
  • Mice, Knockout
  • Models, Genetic
  • Mutation
  • Phenotype
  • Protein Isoforms
  • Sodium
  • TRPM Cation Channels
  • Transient Receptor Potential Channels
  • Vestibular Diseases