FXYD Proteins: New Tissue‐ and Isoform‐Specific Regulators of Na,K‐ATPase

No abstract is available for this paper.

• Publication year

  2003

• Venue

  Annals of the New York Academy of Sciences

• Publication date

  2003-04-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1111/j.1749-6632.2003.tb07219.xPMID 12763855
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Distinct regulatory effects of the Na,K-ATPase gamma subunit.

  2002cited by this paper
• Differential role of KIR channel and Na(+)/K(+)-pump in the regulation of extracellular K(+) in rat hippocampus.

  2002cited by this paper
• Phospholemman (FXYD1) associates with Na,K-ATPase and regulates its transport properties

  2002cited by this paper
• FXYD7 is a brain-specific regulator of Na,K-ATPase alpha 1-beta isozymes.

  2002cited by this paper
• Differential Regulation of Renal Na,K-ATPase by Splice Variants of the γ Subunit*

  2002cited by this paper
• Distinct Regulatory Effects of the Na,K-ATPase γ Subunit*

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• FXYD7 is a brain‐specific regulator of Na,K‐ATPase α1–β isozymes

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• Membrane topology and immunolocalization of CHIF in kidney and intestine.

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• The Functional Role of β Subunits in Oligomeric P-Type ATPases

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• The functional role of beta subunits in oligomeric P-type ATPases.

  2001cited by this paper
• CHIF, a member of the FXYD protein family, is a regulator of Na,K‐ATPase distinct from the γ‐subunit

  2001cited by this paper
• A new variant of the gamma subunit of renal Na,K-ATPase. Identification by mass spectrometry, antibody binding, and expression in cultured cells.

  2000cited by this paper
• Mechanisms of sodium pump regulation.

  2000cited by this paper
• Transport and Pharmacological Properties of Nine Different Human Na,K-ATPase Isozymes*

  2000cited by this paper
• The FXYD gene family of small ion transport regulators or channels: cDNA sequence, protein signature sequence, and expression.

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• Dominant isolated renal magnesium loss is caused by misrouting of the Na+,K+-ATPase γ-subunit

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  1996cited by this paper
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