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Plos Genetics|July 23, 2013
SLC26A4 targeted to the endolymphatic sac rescues hearing and balance in Slc26a4 mutant miceXiangming Li, Joel D Sanneman, Donald G Harbidge, et al.
Stroke|October 9, 2010
Tumor necrosis factor-α enhances microvascular tone and reduces blood flow in the cochlea via enhanced sphingosine-1-phosphate signalingElias Q Scherer, Jingli Yang, Martin Canis, et al.
Theranostics|November 8, 2019
Gene therapy for hereditary hearing loss by SLC26A4 mutations in mice reveals distinct functional roles of pendrin in normal hearingMin-A Kim, Sung Huhn Kim, Nari Ryu, et al.
BMC Medicine|August 24, 2004
Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse modelPhiline Wangemann, Erin M Itza, Beatrice Albrecht, et al.
World Journal of Otorhinolaryngology|May 12, 2015
SLC26A4 mutation testing for hearing loss associated with enlargement of the vestibular aqueductTaku Ito, Julie Muskett, Parna Chattaraj, et al.
Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology|November 26, 2011
SLC26A4 genotypes and phenotypes associated with enlargement of the vestibular aqueductTaku Ito, Byung Yoon Choi, Kelly A King, et al.
The Journal of Clinical Investigation|October 4, 2011
Mouse model of enlarged vestibular aqueducts defines temporal requirement of Slc26a4 expression for hearing acquisitionByung Yoon Choi, Hyoung-Mi Kim, Taku Ito, et al.
Human Molecular Genetics|September 14, 2014
ILDR1 null mice, a model of human deafness DFNB42, show structural aberrations of tricellular tight junctions and degeneration of auditory hair cellsEva L Morozko, Ayako Nishio, Neil J Ingham, et al.
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