Expression cloning of KCRF, a potassium channel regulatory factor

Tal Keren-Raifman, Tatiana Ivanina, Yona Bismuth, Nathan Dascal*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

By functional coexpression screening of a rat cDNA library in Xenopus oocytes, we have cloned a protein (KCRF: K Channel Regulatory Factor) that reduces currents of several K+ channels: G protein-activated GIRK1/4 (K(ir)3.1/K(ir)3.4), inward rectifier IRK1 (K(ir)2.1), and voltage-dependent K(V)1.1/K(V)β1.1. KCRF did not modulate two other K+ channels: ROMK1 (K(ir)1.1) and GIRK1/2 (K(ir)3.1/K(ir)3.2) and the voltage-dependent L-type Ca2+ channels. Western blot analysis showed that KCRF is ubiquitous in rat tissues. Biochemical and electrophysiological experiments revealed that coexpression of KCRF causes a decrease in the level of expression of IRK1 and K(V)1.1/K(V)β1.1 proteins in the oocytes. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)852-858
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume274
Issue number3
DOIs
StatePublished - 11 Aug 2000

Funding

FundersFunder number
National Institutes of Health
National Institute of General Medical SciencesR01GM056260
United States-Israel Binational Science Foundation96-201

    Keywords

    • Calcium channel
    • G protein
    • Ion channel
    • Protein biosynthesis
    • RNA splicing
    • Xenopus oocyte

    Fingerprint

    Dive into the research topics of 'Expression cloning of KCRF, a potassium channel regulatory factor'. Together they form a unique fingerprint.

    Cite this