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NINDSNIMHNICHDNIDCDNEINIDCRNIANIAAANIDANHGRI NCCIHNIDDKNIEHSCCB

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Investigator

Andrew James Griffith, M.D., Ph.D.


Building 5 Room 2A02

Rockville MD 20850-0000
Office: (301) 402-4216


griffita@mail.nih.gov

Dr. Griffith received his B.S. in Chemistry from the University of California, Davis and both his M.D. and Ph.D. from Yale University in 1992. His graduate work in the Department of Molecular Biophysics and Biochemistry was on the molecular cloning and characterized Ku and the Sm-B proteins. Dr. Griffith completed an Otolaryngology residency at the University of Michigan, and was also a postdoctoral fellow in Human Genetics at the University of Michigan where he worked on the genetic analysis of auditory system development and function. Dr. Griffith joined NIDCD as an Investigator in 2000. His laboratory is exploring the molecular basis of genetic deafness, as well as normal auditory system development, structure, and function.



Our laboratory seeks to understand the molecular mechanisms underlying hereditary deafness and normal auditory function. The laboratory's approach is to use genetic approaches to identify critical genes for auditory system structure, function, or development. We then use a variety of techniques to understand the functions of these genes in the auditory system. Mouse models are utilized for both the identification and characterization of these genes.

The main areas of interest in the lab include understanding the molecular basis of hereditary hearing loss associated with enlargement of the vestibular aqueduct/endolymphatic system of the inner ear. Our model is that the causes of this particular auditory phenotype, which includes Pendred syndrome, is a disruption of inner ear fluid (endolymph) homeostasis. Another project is the identification of the mouse Twirler mutation, which causes inner ear malformations in affected mice. The main effort of our lab is toward the characterization of a novel family of genes, the TMC (TransMembrane Cochlear-expressed) genes. We recently discovered this gene family through the positional cloning of TMC1, in which mutations can cause hereditary deafness in humans and mice.



Clinical Protocol

  • Clinical and Molecular Analysis of Enlarged Vestibular Aqueducts 01-DC-0228

  • Genetic Analysis of Hereditary Disorders of Hearing and Balance 01-DC-0229

    Staff Image
    • Kiyoto Kurima, Ph.D.
      Staff Scientist
      (301) 402-8038

    • Tomoko Makishima, M.D., Ph.D.
      Postdoctoral Fellow
      (301) 402-8038

    • Hong-Joon Park, M.D., Ph.D.
      Senior Research Fellow
      (301) 402-8038

    • Shannon Pryor, M.D.
      Research Fellow

    • Yandan Yang, Ph.D.
      Research Assistant