Publication:
Rab-GAP TBC1D4 (AS160) is dispensable for the renal control of sodium and water homeostasis but regulates GLUT4 in mouse kidney

Date

Date

Date
2015
Journal Article
Published version

Abstract

Abstract

Abstract
The Rab GTPase-activating protein TBC1D4 (AS160) controls trafficking of the glucose transporter GLUT4 in adipocytes and skeletal muscle cells. TBC1D4 is also highly abundant in the renal distal tubule, although its role in this tubule is so far unknown. In vitro studies suggest that it is involved in the regulation of renal transporters and channels such as the epithelial sodium channel (ENaC), aquaporin-2 (AQP2), and the Na(+)-K(+)-ATPase. To assess the physiological role of TBC1D4 in the kidney, wild-type (TBC1D4(+/+)) and TBC1D4-d

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184 since deposited on 2015-12-14
Acq. date: 2025-11-13

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Creators (Authors)

  • Di Chiara, Marianna
    affiliation.icon.alt
  • Glaudemans, Bob
    affiliation.icon.alt
  • Loffing-Cueni, Dominique
    affiliation.icon.alt
  • Odermatt, Alex
    affiliation.icon.alt
  • Al-Hasani, Hadi
    affiliation.icon.alt
  • Devuyst, Olivier
    affiliation.icon.alt
  • Faresse, Nourdine
    affiliation.icon.alt
  • Loffing, Johannes
    affiliation.icon.alt

Journal/Series Title

Journal/Series Title

Journal/Series Title

Volume

Volume

Volume
309

Number

Number

Number
9

Page range/Item number

Page range/Item number

Page range/Item number
F779

Page end

Page end

Page end
F790

Item Type

Item Type

Item Type
Journal Article

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Language

Language

Language
English

Publication date

Publication date

Publication date
2015-11-01

Date available

Date available

Date available
2015-12-14

Publisher

Publisher

Publisher

ISSN or e-ISSN

ISSN or e-ISSN

ISSN or e-ISSN
1522-1466

Additional Information

Additional Information

Additional Information
All journals are free accessible after 12 months via HighWire Press

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OA Status

OA Status
Closed

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Free Access at

Free Access at
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PubMed ID

PubMed ID

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184 since deposited on 2015-12-14
Acq. date: 2025-11-13
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