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  Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development

Chun, J., Koenen, M., Katus, H. A., & Zehelein, J. (2004). Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development. Experimental & molecular medicine, 36(4), 367-371. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15365256.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-153D-1 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-153E-0
Genre: Journal Article
Alternative Title : Expression of the IKr components KCNH2 (rERG) and KCNE2 (rMiRP1) during late rat heart development

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 Creators:
Chun, Julian1, Author              
Koenen, Michael1, 2, Author              
Katus, Hugo A., Author
Zehelein, Joerg2, Author              
Affiliations:
1Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              
2Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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Free keywords: cardiac development; delayed rectifier; ERG; fetal expression; IKr current; MiRP1
 Abstract: To understand molecular mechanisms that regulate formation and maintenance of cardiac IKr (rapidly activating component of the delayed rectifier K+ current), we have investigated the spatiotemporal expression pattern of two rat potassium voltage-gated channels, namely subfamily H (eag-related), member2 (KCNH2) (alias name: rERG) and Isk-related family, member2 (KCNE2) (alias name: rMiRP1) during late embryonic development by means of the in situ hybridization technique. KCNE2 is transcribed predominantly in atrial und ventricular myocardium at stages E14.5-E18.5dpc and only a minor signal emerged in the tongue at E16.5dpc. In contrast, KCNH2 transcripts appeared in a less confined pattern with intense signals in atrial and ventricular myocardium, somites, spinal cord, bowel system, central nervous system and thymus at stages E14.5-E18.5dpc. Non-cardiac expression even exceeds the intensity of the cardiac signal, indicating that KCNH2 contributes to K+ currents in non-cardiac tissue as well. Transcription of the rat b-subunit KCNE2 is present in all regions of the fetal myocardium and co-distributes perfectly with transcription of the pore forming a-subunit KCNH2. It seems likely that KCNH2 and KCNE2 are linked to form cardiac IKr channels, associated to cardiogenesis and cardiomyocyte excitability.

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Language(s): eng - English
 Dates: 2004-07-242004-08-31
 Publication Status: Published in print
 Pages: 5
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 Table of Contents: -
 Rev. Type: Peer
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Title: Experimental & molecular medicine
  Alternative Title : Exp. Mol. Med.
Source Genre: Journal
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Publ. Info: New York : Nature Publishing Group
Pages: - Volume / Issue: 36 (4) Sequence Number: - Start / End Page: 367 - 371 Identifier: ISSN: 1226-3613