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Insulin La insulina inicia sus efectos uniéndose al receptor de insulina (IR), una tirosina quinasa receptora. Esta unión desencadena la autofosforilación del receptor, creando sitios de unión para las proteínas sustrato del receptor de insulina (IRS). Las proteínas IRS fosforiladas activan vías posteriores, principalmente la vía PI3K/Akt, que media la mayoría de los efectos metabólicos de la insulina, incluyendo la translocación de los transportadores de glucosa GLUT4 a la membrana celular.
El insulin signaling cascade is a complex and highly regulated network that controls cellular growth, survival, and metabolism. It begins when insulin binds to the extracellular alpha subunits of the insulin receptor (IR). This causes a conformational change, activating the tyrosine kinase domain located on the intracellular beta subunits. The activated kinase phosphorylates specific tyrosine residues on the opposing beta subunit, a process called autophosphorylation. These phosphotyrosine sites act as recruitment platforms for various adapter proteins, most notably the insulin receptor substrate (IRS) family (IRS1-4). Once docked, IRS proteins are themselves phosphorylated by the IR kinase. This creates binding sites for other signaling molecules containing SH2 domains, such as phosphatidylinositol 3-kinase (PI3K). The recruitment of PI3K to the plasma membrane is a critical step. Activated PI3K phosphorylates the lipid [latex]PIP_2[/latex] (phosphatidylinositol 4,5-bisphosphate) to generate [latex]PIP_3[/latex] (phosphatidylinositol 3,4,5-trisphosphate). [latex]PIP_3[/latex] acts as a second messenger, recruiting and activating other kinases, including PDK1 and Akt (also known as Protein Kinase B). Activated Akt is a central node in the pathway, phosphorylating a multitude of downstream targets to mediate insulin’s effects. A key action of Akt is to promote the translocation of vesicles containing the glucose transporter GLUT4 from the cell’s interior to the plasma membrane in muscle and adipose tissue. This insertion of GLUT4 allows for the rapid uptake of glucose from the bloodstream, lowering blood sugar levels. Akt also promotes glycogen synthesis, protein synthesis, and lipid synthesis, while inhibiting processes like gluconeogenesis and apoptosis.
Vía de transducción de señales de insulina
(Si la fecha es desconocida o no es relevante, por ejemplo "mecánica de fluidos", se proporciona una estimación redondeada de su aparición notable)
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