نتایج جستجو برای: pendrin

تعداد نتایج: 335  

Journal: :American journal of physiology. Renal physiology 2012
Julia Rozenfeld Osnat Tal Orly Kladnitsky Lior Adler Edna Efrati Stephen L Carrithers Seth L Alper Israel Zelikovic

The pendrin/SLC26A4 Cl(-)/HCO(3)(-) exchanger, encoded by the PDS gene, is expressed in cortical collecting duct (CCD) non-A intercalated cells. Pendrin is essential for CCD bicarbonate secretion and is also involved in NaCl balance and blood pressure regulation. The intestinal peptide uroguanylin (UGN) is produced in response to oral salt load and can function as an "intestinal natriuretic hor...

Journal: :Human molecular genetics 2000
D A Scott R Wang T M Kreman M Andrews J M McDonald J R Bishop R J Smith L P Karniski V C Sheffield

The PDS gene encodes a transmembrane protein, known as pendrin, which functions as a transporter of iodide and chloride. Mutations in this gene are responsible for Pendred syndrome and autosomal recessive non-syndromic hearing loss at the DFNB4 locus on chromosome 7q31. A screen of 20 individuals from the midwestern USA with non-syndromic hearing loss and dilated vestibular aqueducts identified...

2013
XIANGMING LI

Mutations of SLC26A4 are the most common cause of the hearing loss associated with enlargement of the vestibular aqueduct. SLC26A4 encodes pendrin, an anion exchanger expressed in the cochlea, the vestibular labyrinth, and the endolymphatic sac of the inner ear. Slc26a4 mice, devoid of pendrin expression, develop an enlarged membranous labyrinth which leads to the failure to develop hearing, th...

Journal: :Journal of immunology 2008
Isao Nakao Sachiko Kanaji Shoichiro Ohta Hidetomo Matsushita Kazuhiko Arima Noriko Yuyama Mutsuo Yamaya Katsutoshi Nakayama Hiroshi Kubo Mika Watanabe Hironori Sagara Kumiya Sugiyama Hiroyuki Tanaka Shuji Toda Hiroaki Hayashi Hiromasa Inoue Tomoaki Hoshino Aya Shiraki Makoto Inoue Koichi Suzuki Hisamichi Aizawa Satoshi Okinami Hiroichi Nagai Mamoru Hasegawa Takeshi Fukuda Eric D Green Kenji Izuhara

Excessive production of airway mucus is a cardinal feature of bronchial asthma and chronic obstructive pulmonary disease (COPD) and contributes to morbidity and mortality in these diseases. IL-13, a Th2-type cytokine, is a central mediator in the pathogenesis of bronchial asthma, including mucus overproduction. Using a genome-wide search for genes induced in airway epithelial cells in response ...

Journal: :Endocrinology 2000
I E Royaux K Suzuki A Mori R Katoh L A Everett L D Kohn E D Green

Pendred syndrome is an autosomal recessive disorder characterized by congenital deafness and thyroid goiter. The thyroid disease typically develops around puberty and is associated with a mild organification defect, characterized by an inappropriate discharge of iodide upon perchlorate stimulation (a positive perchlorate discharge test). The gene (PDS) mutated in Pendred syndrome is expressed i...

Journal: :Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2012
Lisann Pelzl Tatsiana Pakladok Ganesh Pathare Hajar Fakhri Diana Michael Carsten A Wagner Markus Paulmichl Florian Lang

BACKGROUND/AIMS Pendrin (SLC26A4), a transporter accomplishing anion exchange, is expressed in inner ear, thyroid gland, kidneys, lung, liver and heart. Loss or reduction of function mutations of SLC26A4 underlie Pendred syndrome, a disorder invariably leading to hearing loss with enlarged vestibular aqueducts and in some patients to hypothyroidism and goiter. Renal pendrin expression is up-reg...

Journal: :American journal of physiology. Cell physiology 2016
Jamile Calil-Silveira Caroline Serrano-Nascimento Peter Andreas Kopp Maria Tereza Nunes

Adequate iodide supply and metabolism are essential for thyroid hormones synthesis. In thyrocytes, iodide uptake is mediated by the sodium-iodide symporter, but several proteins appear to be involved in iodide efflux. Previous studies demonstrated that pendrin is able to mediate apical efflux of iodide in thyrocytes. Acute iodide excess transiently impairs thyroid hormone synthesis, a phenomeno...

Journal: :Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2011
Julia Rozenfeld Edna Efrati Lior Adler Osnat Tal Stephen L Carrithers Seth L Alper Israel Zelikovic

Pendrin (SLC26A4), a Cl(-)/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid and inner ear epithelia and is essential for bicarbonate secretion/chloride reabsorption, iodide accumulation and endolymph ion balance, respectively. The molecular mechanisms controlling pendrin activity in renal, thyroid and inner ear epithelia have been the subject of recent studies...

Journal: :American journal of physiology. Renal physiology 2007
Carsten A Wagner

RENAL REABSORPTION OF SODIUM and chloride is tightly linked in most segments, often occurring even through the same transport proteins such as the Na-K-2Cl cotransporter NKCC2 or the Na-Cl cotransporter NCC in the thick ascending limb or the distal tubule, respectively (1, 6). In the proximal tubule and in parts of the collecting system, the transport of chloride and sodium is mediated by separ...

Journal: :Hypertension 2003
Jill W Verlander Kathryn A Hassell Ines E Royaux Dawn M Glapion Mou-Er Wang Lorraine A Everett Eric D Green Susan M Wall

Pendrin is an anion exchanger expressed along the apical plasma membrane and apical cytoplasmic vesicles of type B and of non-A, non-B intercalated cells of the distal convoluted tubule, connecting tubule, and cortical collecting duct. Thus, Pds (Slc26a4) is a candidate gene for the putative apical anion-exchange process of the type B intercalated cell. Because apical anion exchange-mediated tr...

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