Linked Life Data

21468601

Source:http://linkedlifedata.com/resource/pubmed/id/21468601

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-4-6
pubmed:abstractText
The aim of this study was to investigate whether the early endosome antigen 1 (EEA1) and/or PI3K pathway is involved in the molecular mechanisms underlying the effects of the six-transmembrane protein of prostate 4 (STEAP4; also called STAMP2 and TIARP) on the insulin sensitivity of human adipocytes. Our data demonstrated that siRNA-mediated STEAP4 deficiency significantly decreased insulin-stimulated glucose transport in mature human adipocytes by decreasing GLUT4 translocation to the plasma membrane through attenuated Akt phosphorylation. We further found that EEA1 may not be involved in the mechanisms underlying the effects of STEAP4 on insulin-stimulated glucose uptake and GLUT4 translocation, as indicated by the results that i) STEAP4 does not alter the effects of EEA1 on insulin-stimulated glucose uptake and GLUT4 translocation; ii) STEAP4 does not modify the expression of EEA1 protein; and iii) STEAP4 does not interact with EEA1 according to FRET analysis. In conclusion, this study revealed that the knockdown of STEAP4 inhibits insulin-stimulated glucose transport and GLUT4 translocation via the attenuated phosphorylation of Akt, independent of the effects of EEA1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1791-3004
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
519-23
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:articleTitle
Knockdown of STEAP4 inhibits insulin-stimulated glucose transport and GLUT4 translocation via attenuated phosphorylation of Akt, independent of the effects of EEA1.
pubmed:affiliation
Department of Newborn Infants, Nanjing Children's Hospital of Nanjing Medical University, Nanjing 210008, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't