File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Cardiac Nav1.5 channels are modulated by epidermal growth factor receptor tyrosine kinase

TitleCardiac Nav1.5 channels are modulated by epidermal growth factor receptor tyrosine kinase
Authors
Issue Date2009
PublisherHong Kong Academy of Medicine
Citation
14th Medical Research Conference, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. S1, p. 41 How to Cite?
AbstractIntroduction: Nav1.5 is the pore-forming α-subunit protein of the cardiac sodium channels which plays a pivotal role in the initiation and propagation of the cardiac action potential. It is generally believed that cardiac sodium current (INa) is regulated by protein phosphorylation. Methods: The present study was designed to determine whether protein tyrosine kinases (PTKs) regulate human cardiac Nav1.5 channels stably expressed in HEK 293 cells using a whole-cell patch clamp technique. Results: It was found that human cardiac INa was enhanced by epidermal growth factor (EGF, 100 ng/mL) or the protein tyrosine phosphatases (PTPs) inhibitor orthovanadate (1 mM). The selective EGFR kinase inhibitor AG556 (5 µM) remarkably inhibited INa amplitude, shifted the inactivation voltage toward negative potentials, and slowed the recovery of INa from inactivation. These effects were antagonised by orthovanadate. However, insulin and the Src-family tyrosine kinase inhibitor PP2 had no significant effect on INa. Conclusion: These results suggest that EGFR kinase and PTPs regulate human cardiac Nav1.5 channels stably expressed in HEK-293 cells. EGFR kinase positively, while PTPs negatively modulates the channels. Additional experiments are required to confirm tyrosine phosphorylation level of Nav1.5 using immunoprecipitation and western blot analysis and to find out the tyrosine phosphorylation site(s) of Nav1.5 by site-directed mutagenesis.
Persistent Identifierhttp://hdl.handle.net/10722/62313
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2010-07-13T03:58:36Z-
dc.date.available2010-07-13T03:58:36Z-
dc.date.issued2009en_HK
dc.identifier.citation14th Medical Research Conference, Hong Kong, 10 January 2009. In Hong Kong Medical Journal, 2009, v. 15 n. S1, p. 41-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/62313-
dc.description.abstractIntroduction: Nav1.5 is the pore-forming α-subunit protein of the cardiac sodium channels which plays a pivotal role in the initiation and propagation of the cardiac action potential. It is generally believed that cardiac sodium current (INa) is regulated by protein phosphorylation. Methods: The present study was designed to determine whether protein tyrosine kinases (PTKs) regulate human cardiac Nav1.5 channels stably expressed in HEK 293 cells using a whole-cell patch clamp technique. Results: It was found that human cardiac INa was enhanced by epidermal growth factor (EGF, 100 ng/mL) or the protein tyrosine phosphatases (PTPs) inhibitor orthovanadate (1 mM). The selective EGFR kinase inhibitor AG556 (5 µM) remarkably inhibited INa amplitude, shifted the inactivation voltage toward negative potentials, and slowed the recovery of INa from inactivation. These effects were antagonised by orthovanadate. However, insulin and the Src-family tyrosine kinase inhibitor PP2 had no significant effect on INa. Conclusion: These results suggest that EGFR kinase and PTPs regulate human cardiac Nav1.5 channels stably expressed in HEK-293 cells. EGFR kinase positively, while PTPs negatively modulates the channels. Additional experiments are required to confirm tyrosine phosphorylation level of Nav1.5 using immunoprecipitation and western blot analysis and to find out the tyrosine phosphorylation site(s) of Nav1.5 by site-directed mutagenesis.-
dc.languageengen_HK
dc.publisherHong Kong Academy of Medicine-
dc.relation.ispartofHong Kong Medical Journal-
dc.titleCardiac Nav1.5 channels are modulated by epidermal growth factor receptor tyrosine kinaseen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLau, CP: cplau@hku.hken_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.identifier.hkuros154271en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats