File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Regulation of human cardiac KCNQ1/KCNE1 channel by epidermal growth factor receptor kinase

TitleRegulation of human cardiac KCNQ1/KCNE1 channel by epidermal growth factor receptor kinase
Authors
KeywordsElectrophysiology
Epidermal growth factor receptor kinase
Protein tyrosine phosphorylation
Recombinant cardiac hKCNQ1/hKCNE1 channel
Issue Date2010
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamem
Citation
Biochimica Et Biophysica Acta - Biomembranes, 2010, v. 1798 n. 5, p. 995-1001 How to Cite?
AbstractThe aim of the present study was to investigate whether/how the recombinant human cardiac I Ks could be regulated by epidermal growth factor receptor kinase in HEK 293 cells stably expressing hKCNQ1/hKCNE1 genes using the approaches of perforated patch clamp technique, immunoprecipitation and Western blot analysis. It was found that the broad spectrum isoflavone tyrosine kinase inhibitor genistein and the selective epidermal growth factor receptor kinase inhibitor tyrphostin AG556 suppressed the recombinant I Ks, and their inhibition was countered by the protein tyrosine phosphatase inhibitor orthovanadate. The Src-family kinase inhibitor PP2 reduced the current, but the effect was not antagonized by orthovanadate. Immunoprecipitation and Western blot analysis revealed that tyrosine phosphorylation level of hKCNQ1 protein was decreased by genistein or AG556, but not by PP2. These results provide the novel information that epidermal growth factor receptor kinase, but not Src-family kinases, regulates the recombinant cardiac I Ks stably expressed in HEK 293 cells via phosphorylating KCNQ1 protein of the channel. © 2009 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77635
ISSN
2015 Impact Factor: 3.687
2015 SCImago Journal Rankings: 1.769
ISI Accession Number ID
Funding AgencyGrant Number
Sun Chieh Yeh Heart Foundation of Hong Kong
Funding Information:

The study was supported by a grant from Sun Chieh Yeh Heart Foundation of Hong Kong. The authors thank Mr. Wentao Li for the critical reading of the manuscript.

References

 

DC FieldValueLanguage
dc.contributor.authorDong, MQen_HK
dc.contributor.authorSun, HYen_HK
dc.contributor.authorTang, Qen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-09-06T07:34:03Z-
dc.date.available2010-09-06T07:34:03Z-
dc.date.issued2010en_HK
dc.identifier.citationBiochimica Et Biophysica Acta - Biomembranes, 2010, v. 1798 n. 5, p. 995-1001en_HK
dc.identifier.issn0005-2736en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77635-
dc.description.abstractThe aim of the present study was to investigate whether/how the recombinant human cardiac I Ks could be regulated by epidermal growth factor receptor kinase in HEK 293 cells stably expressing hKCNQ1/hKCNE1 genes using the approaches of perforated patch clamp technique, immunoprecipitation and Western blot analysis. It was found that the broad spectrum isoflavone tyrosine kinase inhibitor genistein and the selective epidermal growth factor receptor kinase inhibitor tyrphostin AG556 suppressed the recombinant I Ks, and their inhibition was countered by the protein tyrosine phosphatase inhibitor orthovanadate. The Src-family kinase inhibitor PP2 reduced the current, but the effect was not antagonized by orthovanadate. Immunoprecipitation and Western blot analysis revealed that tyrosine phosphorylation level of hKCNQ1 protein was decreased by genistein or AG556, but not by PP2. These results provide the novel information that epidermal growth factor receptor kinase, but not Src-family kinases, regulates the recombinant cardiac I Ks stably expressed in HEK 293 cells via phosphorylating KCNQ1 protein of the channel. © 2009 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamemen_HK
dc.relation.ispartofBiochimica et Biophysica Acta - Biomembranesen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Biochimica et Biophysica Acta (BBA) - Biomembranes. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Biochimica et Biophysica Acta (BBA) - Biomembranes, 2010, v. 1798 n. 5, p. 995-1001. DOI: http://dx.doi.org/10.1016/j.bbamem.2010.01.010-
dc.subjectElectrophysiologyen_HK
dc.subjectEpidermal growth factor receptor kinaseen_HK
dc.subjectProtein tyrosine phosphorylationen_HK
dc.subjectRecombinant cardiac hKCNQ1/hKCNE1 channelen_HK
dc.subject.meshCell Line-
dc.subject.meshElectrophysiology-
dc.subject.meshKCNQ1 Potassium Channel - genetics - metabolism-
dc.subject.meshReceptor, Epidermal Growth Factor - antagonists and inhibitors - genetics - metabolism-
dc.subject.meshRecombinant Proteins - genetics - metabolism-
dc.titleRegulation of human cardiac KCNQ1/KCNE1 channel by epidermal growth factor receptor kinaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0005-2736&volume=1798&issue=5&spage=995&epage=1001&date=2010&atitle=Regulation+of+human+cardiac+KCNQ1/KCNE1+channel+by+epidermal+growth+factor+receptor+kinaseen_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.bbamem.2010.01.010en_HK
dc.identifier.pmid20085748-
dc.identifier.scopuseid_2-s2.0-77949263580en_HK
dc.identifier.hkuros168824en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77949263580&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1798en_HK
dc.identifier.issue5en_HK
dc.identifier.spage995en_HK
dc.identifier.epage1001en_HK
dc.identifier.isiWOS:000276648800015-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridDong, MQ=7202127303en_HK
dc.identifier.scopusauthoridSun, HY=35723049200en_HK
dc.identifier.scopusauthoridTang, Q=40861778800en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats