PIP4Ks SUPPRESS INSULIN SIGNALING AND ENHANCE IMMUNE FUNCTION THROUGH A CATALYTIC-INDEPENDENT MECHANISM
AssigneeCornell University
InventorsLewis C. Cantley, Marcia Noreen Paddock, Diana Grace Wang
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Abstract
As described herein, phosphatidylinositol-5-phosphate 4-kinases (PIP4Ks) have an allosteric function in addition to their catalytic activity. The allosteric function suppresses PIP5K-mediated PI(4,5)P2 synthesis and insulin-dependent conversion to PI(3,4,5)P3. Further described herein are methods for treatment of diabetes, metabolic syndrome, insulin resistance, a obesity, cancer, immune deficiency, autoimmune disease, infection, or a combination thereof.
Claims29
A method comprising degrading, modifying, or inhibiting one or more phosphatidylinositol-5-phosphate 4-kinase (PIP4K) isoform(s) in a mammalian subject, or in a population of mammalian cells, to generate a subject with a population of modified mammalian cells, or a population of modified mammalian cells.
A kit comprising one or more binding moieties that specifically binds to at least one phosphatidylinositol-5-phosphate 4-kinase, and instructions for administering one or more of the binding moieties, wherein the binding moiety is directly or indirectly linked to an agent that signals cells to degrade a phosphatidylinositol-5-phosphate 4-kinase bound to the agent.
Use of a phosphatidylinositol-5-phosphate 4-kinase comprising a mutation in sequence VMLXPDD (SEQ ID NO:96, where X is any amino acid), for treatment of diabetes, metabolic syndrome, insulin resistance, obesity, cancer, or a combination thereof.
Use of antibody, nucleic acid inhibitor, or small molecule inhibitor of one or more phosphatidylinositol-5-phosphate 4-kinase isoforms for treatment of diabetes, metabolic syndrome, insulin resistance, obesity, cancer, or a combination thereof.
Dependencies are inferred from the claim text.