Van Denderen, K.
Czech and S. IRS1 knockout mice were growth retarded, but an increase in insulin secretion prevented development of diabetes [ 48 ].
Identification of Promoter Regulatory Elements To understand how the metabolic environment influences GLUT4 gene transcription, it first necessary to identify the molecular elements cis -DNA sequences and trans -acting factors that regulate the gene. H976—H982, 2002.
This important shift in understanding, that the docking and fusion steps may be the key inputs of insulin signaling may lead to understanding the limiting interaction between insulin-signaling pathways and GLUT4 translocation. Sequence and structure of a human glucose transporter. Thus, the signaling cascades responsible for exercise-induced gene expression remain unknown.
Ramm, J. McGee, E. Brown, J. Hashiramoto and D.
An internal deletion of only Domain I was also not expressed in mice Figure 1 , construct 4, and [ 138 ]. Ramalingam et al. Charron, F. The fate of GLUT4-mediated glucose flux in skeletal muscle appears to be metabolized through glycolysis and glycogen synthesis, at least in mice engineered to moderately overexpression the human GLUT4 gene [ 90 ].
Adipose tissue in these animals have upregulated expression of the carbohydrate response element binding protein ChREBP beta-isoform which converts excess dietary carbohydrate to fat in these mice [ 106 ].
In the case of GLUT4 , we have observed a complex pattern of gene expression in various physiologic states, which are not possible to represent in tissue culture models. Interestingly, there was no compensatory glucose uptake mechanism invoked in the GLUT4 null mice subjected to hypoxia, while the bout of swimming did increase muscle-specific glucose uptake in the null mice [ 97 , 98 ].
Kang, J. Proteins matched 175.
Akt activation upon membrane recruitment is dependent on two phosphorylation events, one on threonine 308 and one a serine 473.