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Insulin interacts with the to activate a phosphorylation cascade that begins in the tyrosine kinase domain of the hormone receptor (IR). Glucose is then introduced into the cell as a result.
What are receptors?
Receptors are protein-based chemical structures used in biochemistry and pharmacology that receive and translate signals that may be incorporated into biological systems. These signals often take the form of chemical messengers that attach to receptors and trigger a cellular or tissue response, such as a change in a cell's electrical activity. Relay of signal, amplification, or integration are the three primary subcategories of receptor action. The signal can be transmitted further by relaying, amplified by a single ligand to have a greater effect, and integrated into another metabolic pathway.
Insulin is an anabolic peptide hormone that is secreted by the b cells of the pancreas. It works by binding to a receptor on the membrane of target cells, the most important of which are the liver (where it encourages the storage of glucose as glycogen and reduces glucose output), skeletal muscle, and fat (where it stimulates glucose transport by translocating GLUT4), as well as b cells, brain cells, and actually most cells, where it has pleiotropic.
All metazoans have orthologues of the receptor, which is a member of the receptor tyrosine kinase superfamily. The "apo-receptor," or unbound extracellular domain, has a known structure. Insulin crosslinks the two receptor halves to establish a high affinity by binding to two different locations on each a subunit of the receptor. In addition, the structures of the active and inactive tyrosine kinases have been determined, indicating how an autoinhibitory loop is activated by phosphorylation.
The classical PI3K and ERK cascades, IRS proteins, and a complex intracellular signaling network are all activated by the receptor. The involvement of several signaling proteins in causing the type 2 diabetes phenotype has been investigated using general and tissue-specific targeted gene disruption in mice, with some unexpected results. By integrating the roles of molecules like IRS2 and FOXO, which stop b cell dedifferentiation, insulin signaling in the liver and b cell is emerging as the key factor in type 2 diabetes prevention.
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