Generation and analyses of R8L barttin knockin mouse (Q56974878)

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title

Generation and analyses of R8L barttin knockin mouse (English)

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1

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Thomas Jentsch

16

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author name string

Masato Tajima

2

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Noriko Sugawara

3

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Tetsuji Morimoto

4

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Yoshiaki Kondo

5

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Mayuko Ohno

6

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Keiko Uchida

7

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Kerim Mutig

8

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Sebastian Bachmann

9

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Manoocher Soleimani

10

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Eriko Ohta

11

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Akihito Ohta

12

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Eisei Sohara

13

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Tomokazu Okado

14

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Tatemitsu Rai

15

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Sei Sasaki

17

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Shinichi Uchida

18

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publication date

18 May 2011

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American Journal of Physiology - Renal Physiology

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published in

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volume

301

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issue

2

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page(s)

F297-307

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

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cites work

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Genetics and phenomics of Pendred syndrome

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Phenotype-genotype correlation in antenatal and neonatal variants of Bartter syndrome

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Mouse model of type II Bartter's syndrome. I. Upregulation of thiazide-sensitive Na-Cl cotransport activity

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Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects

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Barttin is a Cl- channel beta-subunit crucial for renal Cl- reabsorption and inner ear K secretion

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Molecular mechanisms of Bartter syndrome caused by mutations in the BSND gene

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Disease-causing dysfunctions of barttin in Bartter syndrome type IV

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Mutations in the chloride channel gene, CLCNKB, leading to a mixed Bartter-Gitelman phenotype

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The Na -dependent chloride-bicarbonate exchanger SLC4A8 mediates an electroneutral Na reabsorption process in the renal cortical collecting ducts of mice

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Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis

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

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A Transgenic Mouse Line That Retains Cre Recombinase Activity in Mature Oocytes Irrespective of thecreTransgene Transmission

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Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats

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Barttin modulates trafficking and function of ClC-K channels

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Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III

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Pathogenesis and treatment of autosomal-dominant nephrogenic diabetes insipidus caused by an aquaporin 2 mutation

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Pendrin: an apical Cl-/OH-/HCO3- exchanger in the kidney cortex

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Localization and functional characterization of rat kidney-specific chloride channel, ClC-K1

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Localization and induction by dehydration of ClC-K chloride channels in the rat kidney.

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Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins

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Barttin increases surface expression and changes current properties of ClC-K channels

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Hsp90 inhibitor partially corrects nephrogenic diabetes insipidus in a conditional knock-in mouse model of aquaporin-2 mutation

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Identifiers

DOI

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