نتایج جستجو برای: ژن slc26a4

تعداد نتایج: 16206  

2016
Giulia Gorrieri Paolo Scudieri Emanuela Caci Marco Schiavon Valeria Tomati Francesco Sirci Francesco Napolitano Diego Carrella Ambra Gianotti Ilaria Musante Maria Favia Valeria Casavola Lorenzo Guerra Federico Rea Roberto Ravazzolo Diego Di Bernardo Luis J. V. Galietta

Goblet cell hyperplasia, a feature of asthma and other respiratory diseases, is driven by the Th-2 cytokines IL-4 and IL-13. In human bronchial epithelial cells, we find that IL-4 induces the expression of many genes coding for ion channels and transporters, including TMEM16A, SLC26A4, SLC12A2, and ATP12A. At the functional level, we find that IL-4 enhances calcium- and cAMP-activated chloride/...

Journal: :Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2011
Aigerim Bizhanova Peter Kopp

Pendred syndrome is an autosomal recessive disorder defined by sensorineural deafness, goiter and a partial organification defect of iodide. It is caused by biallelic mutations in the multifunctional anion transporter pendrin/SLC26A4. In human thyroid tissue, pendrin is localized at the apical membrane of thyroid follicular cells. The clinical phenotype of patients with Pendred syndrome and the...

2012
Shin-Ichi Usami Maiko Miyagawa Shin-Ya Nishio Hideaki Moteki Yutaka Takumi Mika Suzuki Yoko Kitano Satoshi Iwasaki

CONCLUSIONS CDH23 mutations and the 1555A>G mitochondrial mutation were identified among our series of electric acoustic stimulation (EAS) patients, confirming that these genes were important in hearing loss with involvement of high frequency. Successful hearing preservation as well as good outcomes from EAS indicated that patients with this combination of mutations are good candidates for EAS....

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید