3-kinase orchestrates autophagosome formation in yeast.
For example, the ULK1-ATG13-FIP200-ATG101 complex is responsible for the induction of autophagy [16, 17], the class III phosphatidylinositol (PtdIns
) 3-kinase complex (BECN1, ATG14/ATG14L, VPS15, VPS34, and AMBRA1) is responsible for the initiation of the autophagosome [18, 19], and the ATG12-5-16 and LC3-II are responsible for the formation of autophagosome [20-22].
Insall, "Chemotaxis in shallow gradients is mediated independently of PtdIns
3-kinase by biased choices between random protrusions," Nature Cell Biology, vol.
The activation of PI3K by growth factors and nutrients, such as glucose and amino acids, further increases the cellular levels of phosphatidylinositol-3, 4-biphosphate (PtdIns
(4,5) [P.sub.2]) and PtdIns-3, 4, 5-triphosphate (PtdIns
Phosphatidylinositol (PtdIns) is a precursor of arachidonic acid, an intermediate in prostaglandins synthesis.
The PtdIns signaling pathway through inositol triphosphate (insP3) seems to regulate this oocyte maturation stage [58,59].
(13.) Greenwood, JA, Theibert, AB, Prestwich, GD, Murphy-Ullrich, JE, "Restructuring of Focal Adhesion Plaques by PI 3-kinase: Regulation by Ptdins
(3,4,5)-p-3 Binding to Alpha-Actinin." J.
After further refining the system, the researchers concluded that a single phospholipid is responsible: phosphatidylinositol (PtdIns
), which in purified form can protect in concentrations as low as 2.5 percent of the total phospholipid content of membranes.
This decreases intracellular PtdIns
levels and affects the downstream Akt signal transduction pathway.
Figure 7 shows the immunoblot analysis of the low-speed Triton insoluble cytoskeletal fraction of nickel-stimulated platelets using a polyclonal antibody directed against the p85 subunit of PIK, closely correlated with PtdIns
3-kinase enzymatic activity in platelets (18).
Earlier in the decade, several laboratories found that lithium affected a complex biochemical system--called the phosphatidylinositol cycle, or the "PtdIns
cycle' --inside many types of cells.
The genetic mutations in PH domain have been previously reported to interfere with correct localization and sensitivity towards the PtdIns
and have led to major consequences to its functional behaviour .