作者: Ari Elson
DOI: 10.1007/978-1-4614-7855-3_10
关键词:
摘要: The obesity pandemic has focused attention in recent years to the physiological and molecular mechanisms that regulate body weight glucose metabolism. Key signaling pathways both parameters depend heavily on reversible phosphorylation of proteins tyrosine residues, a process regulated by opposing activities kinases phosphatases. Here we review roles protein phosphatase epsilon (PTPe) regulating leptin insulin through them—body Mice lacking PTPe are leptin-hypersensitive protected from gain follows high-fat diet. helps downregulate receptor hypothalamus dephosphorylating JAK2 following activation receptor, thus inhibiting post-activation. is induced perform this function after undergoing receptor-induced at its C-terminal Y695. also insulin-hypersensitive, indicating downregulates as well. Studies muscle cells confirm inhibits signaling, possibly targeting itself. These studies identify inhibitor factor supporting resistance established type-II diabetes, respectively.