Linked Life Data

18976636

Source:http://linkedlifedata.com/resource/pubmed/id/18976636

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-11-25
pubmed:abstractText
The renal inward rectifier potassium channel Kir7.1 has been proposed to be functionally important for tubular K(+) recycling and secretion. This study investigated the regulation of Kir7.1 by PKA and PKC. Cloned human Kir7.1 channels were expressed heterologously in Xenopus oocytes. After pharmacological PKC activation, Kir7.1 currents were strongly inhibited. Co-application of PKC inhibitors attenuated this effect. Inactivation of PKC consensus sites also strongly attenuated the effect with a single site ((201)S) being essential for almost the total PKC sensitivity. In contrast, PKA activation induced an increase of Kir7.1 currents. This effect was absent in mutant Kir7.1 channels lacking PKA consensus site (287)S. In summary, this study demonstrates the dual regulation of Kir7.1 channel function by PKA and PKC. Structurally, these regulations depend on two key residues in the C-terminal channel domain ((Ser)201 for PKC and (Ser)287 for PKA).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
377
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
981-6
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Dual regulation of renal Kir7.1 potassium channels by protein Kinase A and protein Kinase C.
pubmed:affiliation
Department of Nephrology, Renal Center Heidelberg, Im Neuenheimer Feld 162, D-69120 Heidelberg, Germany. wzhang@ix.urz.uni-heidelberg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't