Linked Life Data

20857843

Source:http://linkedlifedata.com/resource/pubmed/id/20857843

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2010-9-22
pubmed:abstractText
In pancreatic beta cells, ATP-sensitive potassium (K(ATP)) channels are metabolic sensors that couple cell metabolism to electrical activity, and therefore K(ATP) channels regulate insulin secretion. We assume that down-regulating the expression of Kir6.2 subunits of K(ATP) channels may change calcium influx induced by glucose and insulin secretion regulated by K(ATP) channels. In our study, we employ Kir6.2-shRNA plasmid to downregulate Kir6.2 expression in HIT-T15 cells. Then, we research the effect of downregulation of Kir6.2 on K(ATP) current, cytoplasmic free Ca2+ concentration and insulin secretion. All results illustrate that downregulation of Kir6.2 subunits of K(ATP) channels in HIT-T15 cells affects K(ATP) current and insulin secretion, and fails to promote calcium influx. The results demonstrate the function of Kir6.2 subunits in electrophysiology characteristic, insulin secretion and calcium influx, and RNA interference provides a feasible alternative to study the function of Kir6.2 subunits in K(ATP) channels in different kinds of diabetes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0334-018X
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
709-17
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Down-regulation of Kir6.2 affects calcium influx and insulin secretion in HIT-T15 cells.
pubmed:affiliation
Experimental Teaching Center of Life Sciences, Shanghai University School of Life Science, Shanghai University, Shanghai, China. chenfuxue@staff.shu.edu.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't