Phosphoinositide 3-kinase pathways and autophagy require phosphatidylinositol phosphate kinases

  • Adv Biol Regul. 2018 May:68:31-38. doi: 10.1016/j.jbior.2018.02.003.
Suyong Choi  1 ,  Xander Houdek  1 ,  Richard A Anderson  2
Affiliations
  • 1. University of Wisconsin-Madison, School of Medicine and Public Health, 1300 University Avenue, Madison, WI 53706, USA.
  • 2. University of Wisconsin-Madison, School of Medicine and Public Health, 1300 University Avenue, Madison, WI 53706, USA. Electronic address: [email protected].
PMID: 29472147 DOI: 10.1016/j.jbior.2018.02.003
Abstract

Phosphatidylinositol phosphate Kinases (PIPKs) generate a lipid messenger phosphatidylinositol 4,5-bisphosphate (PI4,5P2) that controls essentially all aspects of cellular functions. PI4,5P2 rapidly diffuses in the membrane of the lipid bilayer and does not greatly change in membrane or cellular content, and thus PI4,5P2 generation by PIPKs is tightly linked to its usage in subcellular compartments. Based on this verity, recent study of PI4,5P2 signal transduction has been focused on investigations of individual PIPKs and their underlying molecular regulation of cellular processes. Here, we will discuss recent advances in the study of how PIPKs control specific cellular events through assembly and regulation of PI4,5P2 effectors that mediate specific cellular processes. A focus will be on the roles of PIPKs in control of the phosphoinositide 3-kinase pathway and Autophagy.

Keywords
Autophagy; Phosphatidylinositol 4,5-bisphosphate; Phosphatidylinositol phosphate kinase; Phosphoinositide; Phosphoinositide 3-kinase; Signal transduction.