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A role for calcium/calmodulin kinase in insulin stimulated glucose transport

Previous research has shown that the CAMK (calcium/calmodulin dependent protein kinase) inhibitor, KN62, can lead to reductions in insulin stimulated glucose transport. Although controversial, an L-type calcium channel mechanism has also been hypothesized to be involved in insulin stimulated glucose...

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Bibliographic Details
Published in:Life sciences (1973) 2004-01, Vol.74 (7), p.815-825
Main Authors: Wright, D.C, Fick, C.A, Olesen, J.B, Lim, K, Barnes, B.R, Craig, B.W
Format: Article
Language:English
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Summary:Previous research has shown that the CAMK (calcium/calmodulin dependent protein kinase) inhibitor, KN62, can lead to reductions in insulin stimulated glucose transport. Although controversial, an L-type calcium channel mechanism has also been hypothesized to be involved in insulin stimulated glucose transport. The purpose of this report was to determine if 1) L-type calcium channels and CAMK are involved in a similar signaling pathway in the control of insulin stimulated glucose transport and 2) determine if insulin induces an increase in CAMKII phosphorylation through an L-type calcium channel dependent mechanism. Insulin stimulated glucose transport was significantly (p
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2003.06.041