Endocochlear potential depends on Cl- channels: mechanism underlying deafness in Bartter syndrome IV. - Wikidata - wikimedia - TriplyDB

Endocochlear potential depends on Cl- channels: mechanism underlying deafness in Bartter syndrome IV.

Endocochlear potential depends on Cl- channels: mechanism underlying deafness in Bartter syndrome IV.

http://www.wikidata.org/entity/Q30484470

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Conditional gene expression in the mouse inner ear using Cre-loxP.The unique electrical properties in an extracellular fluid of the mammalian cochlea; their functional roles, homeostatic processes, and pathological significance.Discovery of CLC transport proteins: cloning, structure, function and pathophysiology Disruption of the K+ channel beta-subunit KCNE3 reveals an important role in intestinal and tracheal Cl- transport SLC4A11 prevents osmotic imbalance leading to corneal endothelial dystrophy, deafness, and polyuria.KCNK5 channels mostly expressed in cochlear outer sulcus cells are indispensable for hearing Potassium ion movement in the inner ear: insights from genetic disease and mouse models Physiopathology of the cochlear microcirculation Computational model of a circulation current that controls electrochemical properties in the mammalian cochlea.A mouse model for distal renal tubular acidosis reveals a previously unrecognized role of the V-ATPase a4 subunit in the proximal tubule.Slc4a11 gene disruption in mice: cellular targets of sensorineuronal abnormalities.Genetic spectrum of autosomal recessive non-syndromic hearing loss in Pakistani families.Physiology and pathophysiology of ClC-K/barttin channels.Spinster homolog 2 (spns2) deficiency causes early onset progressive hearing loss.Tryptophan Scanning Mutagenesis Identifies the Molecular Determinants of Distinct Barttin Functions.Vestibular role of KCNQ4 and KCNQ5 K+ channels revealed by mouse models.Molecular basis of DFNB73: mutations of BSND can cause nonsyndromic deafness or Bartter syndrome.Developmental Role of Anoctamin-1/TMEM16A in Ca(2+)-Dependent Volume Change in Supporting Cells of the Mouse Cochlea.Development of form and function in the mammalian cochlea.Ca2+ homeostasis defects and hereditary hearing loss.Treating hearing loss in patients with infantile Bartter syndrome.Cell biology and physiology of CLC chloride channels and transporters.Regulatory-auxiliary subunits of CLC chloride channel-transport proteins.ClC Channels and Transporters: Structure, Physiological Functions, and Implications in Human Chloride Channelopathies.Sorting motifs of the endosomal/lysosomal CLC chloride transporters.Alkaline pH block of CLC-K kidney chloride channels mediated by a pore lysine residue.Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations.Reduced Membrane Insertion of CLC-K by V33L Barttin Results in Loss of Hearing, but Leaves Kidney Function Intact.Dissecting a regulatory calcium-binding site of CLC-K kidney chloride channels I-J loop involvement in the pharmacological profile of CLC-K channels expressed in Xenopus oocytes.Barttin activates ClC-K channel function by modulating gating.Hearing Loss Controlled by Optogenetic Stimulation of Nonexcitable Nonglial Cells in the Cochlea of the Inner Ear A regulatory calcium-binding site at the subunit interface of CLC-K kidney chloride channels.Molecular architecture underlying fluid absorption by the developing inner ear Identification of sites responsible for the potentiating effect of niflumic acid on ClC-Ka kidney chloride channels.Expression and immunohistochemical localization of TMEM16A/anoctamin 1, a calcium-activated chloride channel in the mouse cochlea.Deficiency of sphingomyelin synthase-1 but not sphingomyelin synthase-2 causes hearing impairments in mice.Molecular Pharmacology of Kidney and Inner Ear CLC-K Chloride Channels.Carboxyl-terminal Truncations of ClC-Kb Abolish Channel Activation by Barttin Via Modified Common Gating and Trafficking.Residues important for nitrate/proton coupling in plant and mammalian CLC transporters.

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Endocochlear potential depends on Cl- channels: mechanism underlying deafness in Bartter syndrome IV.

http://www.wikidata.org/entity/Q30484470

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2008 nî lūn-bûn

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2008 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2008年の論文

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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The EMBO Journal

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Endocochlear potential depends ...... afness in Bartter syndrome IV.

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Anselm A Zdebik

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Chris I De Zeeuw

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Corina E Andreescu

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Gesa Rickheit

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Hannes Maier

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Nicola Strenzke

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P2860

KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness

Two highly homologous members of the ClC chloride channel family in both rat and human kidney

A novel mutation in the potassium channel gene KVLQT1 causes the Jervell and Lange-Nielsen cardioauditory syndrome

Thyroid hormone is a critical determinant for the regulation of the cochlear motor protein prestin.

The endocochlear potential depends on two K+ diffusion potentials and an electrical barrier in the stria vascularis of the inner ear

Barttin modulates trafficking and function of ClC-K channels

Deafness and imbalance associated with inactivation of the secretory Na-K-2Cl co-transporter

Gap junction systems in the mammalian cochlea

Colocalization of KCNQ1/KCNE channel subunits in the mouse gastrointestinal tract

Mutation of BSND causes Bartter syndrome with sensorineural deafness and kidney failure

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2907-2917

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10.1038/EMBOJ.2008.203

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21

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27

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Chris I De Zeeuw

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2008-10-02T00:00:00Z

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23297759

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18833191

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2580783

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