Defects in the insulin-signaling pathway may lead to the development of skeletal muscle insulin resistance, which is one of the earliest abnormalities detected in individuals with the metabolic syndrome and predisposes them to develop type 2 diabetes. Previous studies have shown that deletion of the mouse sequestosome 1/p62 gene results in mature-onset obesity that progresses to insulin and leptin resistance and, ultimately, type 2 diabetes. Sequestosome 1/p62 is involved in receptor-mediated signal transduction and functions as an intracellular signal modulator or adaptor protein.
View Article and Find Full Text PDFSequestosome 1/p62 is a signal modulator or adaptor protein involved in receptor-mediated signal transduction. Sequestosome 1/p62 is gaining attention as it is involved in several diseases including Parkinson disease, Alzheimer disease, liver and breast cancer, Paget's disease of bone, obesity and insulin resistance. In this review, we will focus on the most recent advances on the physiological function of p62 relevant to human diseases.
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