Zobrazeno 1 - 10
of 124
pro vyhledávání: '"Philine Wangemann"'
Autor:
Keiji Honda, Sung Huhn Kim, Michael C Kelly, Joseph C Burns, Laura Constance, Xiangming Li, Fei Zhou, Michael Hoa, Matthew W Kelley, Philine Wangemann, Robert J Morell, Andrew J Griffith
Publikováno v:
eLife, Vol 6 (2017)
Mutations of SLC26A4 are a common cause of hearing loss associated with enlargement of the endolymphatic sac (EES). Slc26a4 expression in the developing mouse endolymphatic sac is required for acquisition of normal inner ear structure and function. H
Externí odkaz:
https://doaj.org/article/79806d70a13945af8dd52d996a2897bd
Autor:
Taku Ito, Xiangming Li, Kiyoto Kurima, Byung Yoon Choi, Philine Wangemann, Andrew J. Griffith
Publikováno v:
Neurobiology of Disease, Vol 66, Iss , Pp 53-65 (2014)
SLC26A4 mutations can cause a distinctive hearing loss phenotype with sudden drops and fluctuation in patients. Existing Slc26a4 mutant mouse lines have a profound loss of hearing and vestibular function, with severe inner ear malformations that do n
Externí odkaz:
https://doaj.org/article/b20cdf786ace4ee1a4a2cd4a39110611
Autor:
Philine Wangemann
Publikováno v:
Cellular Physiology and Biochemistry, Vol 32, Iss 1, Pp 157-165 (2013)
The human gene SLC26A4 and the mouse ortholog Slc26a4 code for the protein pendrin, which is an anion exchanger expressed in apical membranes of selected epithelia. In the inner ear, pendrin is expressed in the cochlea, the vestibular labyrinth and t
Externí odkaz:
https://doaj.org/article/13254a5683ed43f3a01dbce52a1a579a
Autor:
Kyunghee X Kim, Joel D Sanneman, Hyoung-Mi Kim, Donald G Harbidge, Jie Xu, Manoocher Soleimani, Philine Wangemann, Daniel C Marcus
Publikováno v:
PLoS ONE, Vol 9, Iss 5, p e97191 (2014)
Several members of the SLC26 gene family have highly-restricted expression patterns in the auditory and vestibular periphery and mutations in mice of at least two of these (SLC26A4 and SLC26A5) lead to deficits in hearing and/or balance. A previous r
Externí odkaz:
https://doaj.org/article/a4af9d3081b24515b3e3cae7919f4d65
Publikováno v:
PLoS ONE, Vol 8, Iss 5, p e65977 (2013)
Slc26a4 (Δ/Δ) mice are deaf, develop an enlarged membranous labyrinth, and thereby largely resemble the human phenotype where mutations of SLC26A4 cause an enlarged vestibular aqueduct and sensorineural hearing loss. The enlargement is likely cause
Externí odkaz:
https://doaj.org/article/af1fbac376ce454f9821a1348def763e
Publikováno v:
PLoS ONE, Vol 8, Iss 1, p e53655 (2013)
Cochlear blood flow regulation is important to prevent hearing loss caused by ischemia and oxidative stress. Cochlear blood supply is provided by the spiral modiolar artery (SMA). The myogenic tone of the SMA is enhanced by the nitric oxide synthase
Externí odkaz:
https://doaj.org/article/f81fc56701554f3597dbcc55165690df
Autor:
Xiangming Li, Joel D Sanneman, Donald G Harbidge, Fei Zhou, Taku Ito, Raoul Nelson, Nicolas Picard, Régine Chambrey, Dominique Eladari, Tracy Miesner, Andrew J Griffith, Daniel C Marcus, Philine Wangemann
Publikováno v:
PLoS Genetics, Vol 9, Iss 7, p e1003641 (2013)
Mutations of SLC26A4 are a common cause of human hearing loss associated with enlargement of the vestibular aqueduct. SLC26A4 encodes pendrin, an anion exchanger expressed in a variety of epithelial cells in the cochlea, the vestibular labyrinth and
Externí odkaz:
https://doaj.org/article/a86719aa2c854770b010a3f7775fd156
Autor:
Hyoung-Mi Kim, Philine Wangemann
Publikováno v:
PLoS ONE, Vol 6, Iss 3, p e17949 (2011)
Loss-of-function mutations of SLC26A4/pendrin are among the most prevalent causes of deafness. Deafness and vestibular dysfunction in the corresponding mouse model, Slc26a4(-/-), are associated with an enlargement and acidification of the membranous
Externí odkaz:
https://doaj.org/article/0320782c6b614431b52997c99e0ed094
Publikováno v:
PLoS ONE, Vol 6, Iss 9, p e25659 (2011)
Regulation of cochlear blood flow is critical for hearing due to its exquisite sensitivity to ischemia and oxidative stress. Many forms of hearing loss such as sensorineural hearing loss and presbyacusis may involve or be aggravated by blood flow dis
Externí odkaz:
https://doaj.org/article/22af90adb7bf465bb720f6673ee673f6
Autor:
Hyoung-Mi Kim, Philine Wangemann
Publikováno v:
PLoS ONE, Vol 5, Iss 11, p e14041 (2010)
Mutations of SLC26A4 are among the most prevalent causes of hereditary deafness. Deafness in the corresponding mouse model, Slc26a4(-/-), results from an abnormally enlarged cochlear lumen. The goal of this study was to determine whether the cochlear
Externí odkaz:
https://doaj.org/article/c72b58f9f5ff4118856be0c7246bde2f