File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Involvement of K v1.1 and Na v1.5 in proliferation of gastric epithelial cells

TitleInvolvement of K v1.1 and Na v1.5 in proliferation of gastric epithelial cells
Authors
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010
Citation
Journal Of Cellular Physiology, 2006, v. 207 n. 2, p. 437-444 How to Cite?
AbstractIn the present study, patch clamp experiments demonstrated the expression of multiple ionic currents, including a Ba 2+-sensitive inward rectifier K + current (I Kir), a 4-aminopyridine- (4-AP) sensitive delayed rectifier K + current (IK DR), and a nifedipine-sensitive, tetrodotoxin-resistant inward Na + current (I Na.TTXR) in the non-transformed rat gastric epithelial cell line RGM-1. RT-PCR revealed molecular identities of mRNAs for the functional ionic currents, including K ir1.2 for I Kir, K v1.1, K v1.6, and K v2.1 for IK DR, and Na v1.5 for I Na.TTxR. Pharmacologic blockade of K v and Na v, but not K ir, suppressed RGM-1 cell proliferation. To further elucidate which subtypes of the ion channels were involved in cell proliferation, RNA interference was employed to knockdown specific gene expression. Downregulation of K v1.1 or Na v1.5 by RNA interference suppressed RGM-1 cell proliferation. To conclude, our study is the first to delineate the expression of ion channels and their functions as growth modulators in gastric epithelial cells. © 2005 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/168010
ISSN
2015 Impact Factor: 4.155
2015 SCImago Journal Rankings: 1.842
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWu, WKKen_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorWong, HPSen_US
dc.contributor.authorHui, MKCen_US
dc.contributor.authorTai, EKKen_US
dc.contributor.authorLam, EKYen_US
dc.contributor.authorShin, VYen_US
dc.contributor.authorYe, YNen_US
dc.contributor.authorLi, Pen_US
dc.contributor.authorYang, YHen_US
dc.contributor.authorLuo, JCen_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-10-08T03:14:04Z-
dc.date.available2012-10-08T03:14:04Z-
dc.date.issued2006en_US
dc.identifier.citationJournal Of Cellular Physiology, 2006, v. 207 n. 2, p. 437-444en_US
dc.identifier.issn0021-9541en_US
dc.identifier.urihttp://hdl.handle.net/10722/168010-
dc.description.abstractIn the present study, patch clamp experiments demonstrated the expression of multiple ionic currents, including a Ba 2+-sensitive inward rectifier K + current (I Kir), a 4-aminopyridine- (4-AP) sensitive delayed rectifier K + current (IK DR), and a nifedipine-sensitive, tetrodotoxin-resistant inward Na + current (I Na.TTXR) in the non-transformed rat gastric epithelial cell line RGM-1. RT-PCR revealed molecular identities of mRNAs for the functional ionic currents, including K ir1.2 for I Kir, K v1.1, K v1.6, and K v2.1 for IK DR, and Na v1.5 for I Na.TTxR. Pharmacologic blockade of K v and Na v, but not K ir, suppressed RGM-1 cell proliferation. To further elucidate which subtypes of the ion channels were involved in cell proliferation, RNA interference was employed to knockdown specific gene expression. Downregulation of K v1.1 or Na v1.5 by RNA interference suppressed RGM-1 cell proliferation. To conclude, our study is the first to delineate the expression of ion channels and their functions as growth modulators in gastric epithelial cells. © 2005 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31010en_US
dc.relation.ispartofJournal of Cellular Physiologyen_US
dc.rightsJournal of Cellular Physiology. Copyright © John Wiley & Sons, Inc.-
dc.titleInvolvement of K v1.1 and Na v1.5 in proliferation of gastric epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.emailWong, HPS:hpswong@hkusua.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.identifier.authorityWong, HPS=rp00808en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jcp.20576en_US
dc.identifier.pmid16331678-
dc.identifier.scopuseid_2-s2.0-33645660002en_US
dc.identifier.hkuros112635-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645660002&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume207en_US
dc.identifier.issue2en_US
dc.identifier.spage437en_US
dc.identifier.epage444en_US
dc.identifier.isiWOS:000236651800019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWu, WKK=18345422600en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridWong, HPS=8644138100en_US
dc.identifier.scopusauthoridHui, MKC=8644138500en_US
dc.identifier.scopusauthoridTai, EKK=9842278900en_US
dc.identifier.scopusauthoridLam, EKY=8644138600en_US
dc.identifier.scopusauthoridShin, VY=7003491170en_US
dc.identifier.scopusauthoridYe, YN=34975045800en_US
dc.identifier.scopusauthoridLi, P=26643192100en_US
dc.identifier.scopusauthoridYang, YH=7409390524en_US
dc.identifier.scopusauthoridLuo, JC=7404182407en_US
dc.identifier.scopusauthoridCho, CH=7403100461en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats