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Research

Under the leadership of Dr. Erick Lin, the Department of Otolaryngology's research team is currently studying mechanisms of deafness caused by genetic mutations.  Current projects investigate roles for Gjb2 and Gjb6 genes, which code for intercellular gap junctions.  Mutations in these genes are responsible for about half of babies born deaf.  We also carry out translational studies focusing on (1) clinically applicable diagnostic methods for genetic screening of all known deafness genes and (2) drugs that protect the hair cells and spiral ganglion neurons.

Current Grant Support

  1. NIH RO1 (NIDCD, RO1DC006483), 2005-2015, Title: Role of connexins in cochlear functions
  2. NIH R21/R33 (NIDCD, R21DC010476), 2009-2014, Title: Genetic hearing screening and diagnosis facilitated by using a combined low-cost exon capture and large-scale sequencing approach
  3. NIH R41 (NIDCD, R41DC009713), 2010, Title: Genetic hearing screening for newborns
  4. NIH RO1 (NIDCD, RO1DC010204), 2009-2014, Title: Auditory neuroprotection by small molecule agonists of the TrkB Receptor
  5. NIH R21 (NIDCD, R21DC008353), 2007-2010, Title: Mouse models for human deafness caused by diverse types of connex26 mutations

Techniques Used in the Lab

  1. Generation of transgenic mice
  2. Standard elctrophysiological methods (e.g., patch clamp recording)
  3. Specialized eletrophysiological recordings for hearing functions in mice
  4. Standard molecular biology techniques (e.g., molecular cloning, library preparations, etc.)
  5. Cellular imaging techniques for studying the functions
  6. Immunolabeling and histological methods

Selected Publications

  1. Ahmad S., Tang W.X., Chang Q., Qu Y., Hibshman J., Li Y.H., Sohl G., Willecke K., Chen P., Lin X.  (2007)  Restoration of connexin26 protein level in the cochlea completely rescue hearing in a mouse model of human connexin30-linked deafness.  Proc Natl Acade Sci, 104(4): 1337-1341.  (PMID: 17227867)
  2. Chang Q., Tang W., Ahmad S., Zhou B., Lin X.  (2008)  Gap junction mediated intercellular metabolite transfer in the cochlea is compromised in connexin30 null mice.  PLoS One, 3(12): e4008.  (PMID: 19116647)
  3. Hoang Dinh E., Ahmad S., Chang Q., Tang W., Stong B., Lin X.  (2009) Diverse deafness mechanisms of connexin mutations revealed by studies using in vitro approaches and mouse models.  Invited review paper.  Brain Res., 1277: 52-69.  (doi:10.1016/j.brainres.2009.02.008)  (PMID: 19230829)
  4. Wang YF, Chang Q., Tang W., sun Y., Zhou BF, Li HW, Lin X.  (2009)  Targeted connexin26 ablatoin arrests postnasal development of the organ of Corti.  Biochemical and Biophysical Research Communications, 385(1): 33-7.  (doi: 10.1016/j.bbrc.2009.05/023) (PMID: 19433060)
  5. Jang S-W., Liu X., Chan C.B., France S.A., Sayeed I., Tang W., Lin X., Xiao G., Andero R., Chang Q., Ressler K., Ye K.  (2010)  Deoxygedunin, a natural product with potent neurotrophic activity in mice.  PLoS ONE, 5(7): e11528.  (doi: 10.1371/journal/pone.0011528)