Linked Life Data

18772605

Source:http://linkedlifedata.com/resource/pubmed/id/18772605

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-9-5
pubmed:abstractText
Insulin induces translocation of the glucose transporter GLUT4 from intracellular storage compartment to the plasma membrane via complex mechanisms that require intact cytoskeletal networks. In cultured adipocytes, conventional kinesin motor proteins have been proposed to mediate GLUT4 movements on microtubules. It remains, however, unclear whether kinesin motor system plays a similar regulatory role in myocytes. We addressed this issue using C2C12 myoblasts, which have now been shown to express both heavy and light chains of conventional kinesin. In these cells, overexpression of either wild-type kinesin light chain 2 (KLC2) or its phosphorylation-defective mutant did not significantly affect insulin-stimulated translocation of exofacial Myc-tagged GLUT4-green fluorescent protein to the cell surface and its subsequent externalization. Likewise, a dominant-negative mutant of KLC2 had no marked effect on GLUT4 movements in this cell type. These results suggest that conventional kinesin is dispensable for insulin-induced GLUT4 translocation in cultured myoblasts and may thus reveal a cell-type specific role of the microtubules-based cytoskeleton in glucose transport in response to insulin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1883-0498
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E14-22
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Insulin-induced GLUT4 movements in C2C12 myoblasts: evidence against a role of conventional kinesin motor proteins.
pubmed:affiliation
Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't