Inhibition of cardiac delayed rectifier K+ currents by an antisense oligodeoxynucleotide against IsK (minK) and over-expression of IsK mutant D77N ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-06

AUTHORS

Hideo Ohyama, Hidetoshi Kajita, Koichiro Omori, Toru Takumi, Nobuhiro Hiramoto, Toshiji Iwasaka, Hiroko Matsuda

ABSTRACT

. The IsK (minK or KCNE1) protein is known to co-assemble with the KvLQT1 (KCNQ1) protein to form a channel underlying the slowly activating delayed rectifier K+ current (IKs). Controversy remains as to whether the IsK protein assembles with ERG (the ether-a-go-go-related gene) products to form or modulate the channel underlying the rapidly activating delayed rectifier K+ current (IKr). We investigated the effects of antisense oligodeoxynucleotides (AS-ODN) against IsK and its mutant D77N [which underlies a form of long QT syndrome (LQT5) in humans] on the delayed rectifier K+ current (IK) of neonatal mouse ventricular myocytes in primary culture. Patch-clamp experiments on these cells showed that IK consists of IKs and IKr. IK was not recorded from ventricular cells transfected with AS-ODN, while it was recorded from cells transfected with the corresponding sense oligodeoxynucleotides (S-ODN). IK was not recorded from cells transfected with the D77N mutant, and the action potential duration was much longer than in cells transfected with wild-type IsK. Furthermore, HERG could not induce currents in COS-1 cells co-expressed with the D77N mutant and HERG (the human form of ERG). These results indicate that the IsK protein associates with both KvLQT1 and ERG products to modulate IKr and IKs in cardiac myocytes. More... »

PAGES

329-335

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s004240100547

DOI

http://dx.doi.org/10.1007/s004240100547

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1002823240

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11484762


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