Abstract
GLUT4 is a glucose transporter protein expressed in the heart and translocates from cytoplasm to sarcolemma under ischemia. Hearts from mice with cardiac-selective GLUT4 deficiency develop profound and irreversible dysfunction after ischemia. Therefore, GLUT4 translocation represents protection against ischemic injury. To identify the signaling pathways of myocardial GLUT4 translocation, we established a novel method for quantifying the relative proportion of sarcolemmal GLUT4 to total GLUT4. We constructed a GLUT4 reporter containing a c-Myc epitope tag in the first exofacial loop and fused GFP to the C-terminus in the lenti virus vector.
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