Comparative ontogeny, processing, and segmental distribution of the renal chloride channel, ClC-5 (Q24301875)

Aquaporin 1

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ATPase H+ transporting V0 subunit a4

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Chloride voltage-gated channel 5

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ATPase, H+ transporting, lysosomal V0 subunit A4

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Chloride channel, voltage-sensitive 5

1 reference

7

Olivier Devuyst

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Fiona E Karet

object named as

Fiona E Karet

5

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Rajesh Thakker

object named as

Rajesh V Thakker

6

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François Jouret

1

object named as

François Jouret

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author name string

Takashi Igarashi

2

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Françoise Gofflot

3

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Patricia D Wilson

https://scigraph.springernature.com/pub.10.1111/j.1523-1755.2004.00360.x

4

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language of work or name

English

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publication date

January 2004

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published in

Kidney International

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volume

65

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page(s)

198-208

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issue

1

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exact match

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cites work

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A familial syndrome due to Arg648Stop mutation in the X-linked renal chloride channel gene

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ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease.

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Recombination: a means to an end in human cells

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Mutations in ATP6N1B, encoding a new kidney vacuolar proton pump 116-kD subunit, cause recessive distal renal tubular acidosis with preserved hearing

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Changes in global gene expression patterns during development and maturation of the rat kidney

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ClC-5, the chloride channel mutated in Dent's disease, colocalizes with the proton pump in endocytotically active kidney cells

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Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease

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Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.

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Molecular structure and physiological function of chloride channels

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Ontogeny of CLCN3 chloride channel gene expression in human pulmonary epithelium

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Carbonic anhydrase in the human fetal kidney

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