Insulin stimulated glucose uptake is a critical component of glucose homeostasis. The studies presented here show that myosin IIA is actively recruited to the plasma membrane upon insulin stimulation. I also show that inhibiting the interaction of myosin II with actin or inhibiting the activation of myosin II by myosin light chain kinase resulted in myosin IIA remaining localized to the perinuclear region of 3T3-L1 adipocytes. Based on my findings I hypothesized that the localization and activation of myosin IIA is regulated by the activation of the insulin signaling pathway. The studies presented here reveal underlying interactions and mechanisms affecting insulin stimulated glucose uptake providing important information that can be used to optimize current treatments or develop new treatments for type II diabetes
