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InAKTivation of insulin/IGF-1 signaling by dephosphorylation. | LitMetric

AI Article Synopsis

  • Signal transduction pathways involve cycles of phosphorylation and dephosphorylation, with mammals having more protein kinase genes than phosphatase genes, leading to the need for phosphatases to partner with specific regulatory subunits to target substrate proteins.
  • An example is the C. elegans phosphatase PPTR-1, which negatively influences the insulin signaling pathway, affecting longevity, metabolism, and stress responses by modulating the activity of the kinase AKT.
  • The activation of the FOXO transcription factor DAF-16 through this process highlights the potential of B56 subunit functions in addressing diseases like Type 2 diabetes and cancer, where AKT phosphorylation is disrupted.

Article Abstract

Signal transduction pathways are tightly regulated by phosphorylation-dephosphorylation cycles and yet the mammalian genome contains far more genes that encode for protein kinases than protein phosphatases. Therefore, to target specific substrates, many phosphatases associate with distinct regulatory subunits and thereby modulate multiple cellular processes. One such example is the C. elegans PP2A regulatory subunit PPTR-1 that negatively regulates the insulin/insulin-like growth factor signaling pathway to modulate longevity, dauer diapause, fat metabolism and stress resistance. PPTR-1, as well as its mammalian homolog B56beta, specifically target the PP2A enzyme to AKT and mediate the dephosphorylation of this important kinase at a conserved threonine residue. In C. elegans, the major consequence of this modulation is activation of the FOXO transcription factor homolog DAF-16, which in turn regulates transcription of its many target genes involved in longevity and stress resistance. Understanding the function of B56 subunits may have important consequences in diseases such as Type 2 diabetes and cancer where the balance of Akt phosphorylation is deregulated.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3109867PMC
http://dx.doi.org/10.4161/cc.8.23.10072DOI Listing

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