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FXYD7 is a brain‐specific regulator of Na,K‐ATPase α1–β isozymes
Author(s) -
Béguin Pascal,
Crambert Gilles,
MonnetTschudi Florianne,
Uldry Marc,
Horisberger JeanDaniel,
Garty Haim,
Geering Käthi
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdf330
Subject(s) - biology , isozyme , regulator , beta (programming language) , atpase , enzyme , biochemistry , microbiology and biotechnology , genetics , gene , computer science , programming language
Recently, corticosteroid hormone‐induced factor (CHIF) and the γ‐subunit, two members of the FXYD family of small proteins, have been identified as regulators of renal Na,K‐ATPase. In this study, we have investigated the tissue distribution and the structural and functional properties of FXYD7, another family member which has not yet been characterized. Expressed exclusively in the brain, FXYD7 is a type I membrane protein bearing N‐terminal, post‐translationally added modifications on threonine residues, most probably O ‐glycosylations that are important for protein stabilization. Expressed in Xenopus oocytes, FXYD7 can interact with Na,K‐ATPase α1–β1, α2–β1 and α3–β1 but not with α–β2 isozymes, whereas, in brain, it is only associated with α1–β isozymes. FXYD7 decreases the apparent K + affinity of α1–β1 and α2–β1, but not of α3–β1 isozymes. These data suggest that FXYD7 is a novel, tissue‐ and isoform‐specific Na,K‐ATPase regulator which could play an important role in neuronal excitability.