Document Detail


Cardiac small conductance Ca2+-activated K+ channel subunits form heteromultimers via the coiled-coil domains in the C termini of the channels.
MedLine Citation:
PMID:  20689065     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
RATIONALE: Ca(2+)-activated K(+) channels are present in a wide variety of cells. We have previously reported the presence of small conductance Ca(2+)-activated K(+) (SK or K(Ca)) channels in human and mouse cardiac myocytes that contribute functionally toward the shape and duration of cardiac action potentials. Three isoforms of SK channel subunits (SK1, SK2, and SK3) are found to be expressed. Moreover, there is differential expression with more abundant SK channels in the atria and pacemaking tissues compared with the ventricles. SK channels are proposed to be assembled as tetramers similar to other K(+) channels, but the molecular determinants driving their subunit interaction and assembly are not defined in cardiac tissues.
OBJECTIVE: To investigate the heteromultimeric formation and the domain necessary for the assembly of 3 SK channel subunits (SK1, SK2, and SK3) into complexes in human and mouse hearts.
METHODS AND RESULTS: Here, we provide evidence to support the formation of heteromultimeric complexes among different SK channel subunits in native cardiac tissues. SK1, SK2, and SK3 subunits contain coiled-coil domains (CCDs) in the C termini. In vitro interaction assay supports the direct interaction between CCDs of the channel subunits. Moreover, specific inhibitory peptides derived from CCDs block the Ca(2+)-activated K(+) current in atrial myocytes, which is important for cardiac repolarization.
CONCLUSIONS: The data provide evidence for the formation of heteromultimeric complexes among different SK channel subunits in atrial myocytes. Because SK channels are predominantly expressed in atrial myocytes, specific ligands of the different isoforms of SK channel subunits may offer a unique therapeutic opportunity to directly modify atrial cells without interfering with ventricular myocytes.
Authors:
Dipika Tuteja; Sassan Rafizadeh; Valeriy Timofeyev; Shuyun Wang; Zheng Zhang; Ning Li; Robertino K Mateo; Anil Singapuri; J Nilas Young; Anne A Knowlton; Nipavan Chiamvimonvat
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-08-05
Journal Detail:
Title:  Circulation research     Volume:  107     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-01     Completed Date:  2010-10-22     Revised Date:  2010-12-20    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  851-9     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of California, Davis, CA 95616, USA.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / physiology*
Amino Acid Sequence
Animals
Cells, Cultured
Heart Atria / cytology
Humans
Mice
Molecular Sequence Data
Myocytes, Cardiac / cytology,  physiology*
Patch-Clamp Techniques
Potassium / metabolism*
Protein Multimerization
Protein Structure, Tertiary
Small-Conductance Calcium-Activated Potassium Channels* / chemistry,  genetics,  physiology
Transfection
Grant Support
ID/Acronym/Agency:
HL085844/HL/NHLBI NIH HHS; R01 HL075274/HL/NHLBI NIH HHS; R01 HL085727-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/KCNN1 protein, human; 0/KCNN2 protein, human; 0/KCNN3 protein, human; 0/Kcnn1 protein, mouse; 0/Kcnn2 protein, mouse; 0/Kcnn3 protein, mouse; 0/Small-Conductance Calcium-Activated Potassium Channels; 7440-09-7/Potassium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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