Here's the scientific description: «In this process, the capsaicin receptor (TRPV1) is sensitized
by phosphatidylinositol -4,5-bisphosphate (PIP2) hydrolysis following phospholipase C activation.»
This, in turn, is actually a lipid kinase and it phosphorylates lipids on the plasma membrane, making a new or synthesizing a new phosphate or a lipid
phosphatidylinositol lipid called PIP - 3.
PTEN can also reduce the levels of another similar molecule known
as phosphatidylinositol -3,4-bisphosphate (PI (3,4) P2).
Co-author, «Treatment of A431 Cells with Epidermal Growth Factor (EGF) Induces Desensitization of EGF -
Stimulated Phosphatidylinositol Turnover,» The Journal of Biological Chemistry, 1989
Previously, nucleophosmin - ALK has been shown to
activate phosphatidylinositol 3 - kinase (PI3K) and its downstream effector, the serine / threonine kinase AKT.
Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate - 1 (IRS - 1)-
associated phosphatidylinositol 3 - kinase activity in muscle.
By regulating the levels of the
chemical phosphatidylinositol -3,4,5-trisphosphate (PI (3,4,5) P3), PTEN helps to limit cell growth and so prevents cancer.
We regenerated cells stably expressing ectopic wild - type and
mutant phosphatidylinositol -3,4,5-trisphosphate-dependent Rac exchange factor 2 (PREX2) using the same immortalized human NRASG12D melanocytes as the original study.
Metlakunta AS, Sahu M, Sahu A.
Hypothalamic phosphatidylinositol 3 - kinase pathway of leptin signaling is impaired during the development of diet - induced obesity in FVB / N mice.
This leads to production of this lipid called PIP3 (
phosphatidylinositol trisphosphate), and this, in turn, has been shown to lead to a remodeling of actin, F - actin turning into G - actin.
In what concerns intra-membrane constituents, the focus of interest has been
on phosphatidylinositol lipids and their capacity to orchestrate endocytic events on the cytosolic leaflet of the membrane.
Phosphatidylinositol -3-kinase (PI3K) inhibitors (LY294002 (10 μM) and wortmannin (10 μM)-RRB- and an AKT inhibitor (deguelin (0.1 or 0.2 μM)-RRB- were added to the 293, 293T, HepG2, and Hepa - 1c1c7 cells that had been treated with ActD.
Researchers at the Kyung Hee University in Korea discovered how: like insulin, EGCG [structural formula below] activates the
enzyme phosphatidylinositol (PI) 3 - kinase.
Roles
of phosphatidylinositol 3 - kinase and osteopontin in steatosis and aminotransferase release by hepatocytes treated with methionine - choline - deficient medium.
RESULTS: Short - term treatment of 3T3 - L1 adipocytes with R (+) alpha - lipoic acid rapidly stimulated glucose uptake in a wortmannin - sensitive manner, induced a redistribution of GLUT1 and GLUT4 to the plasma membrane, caused tyrosine phosphorylation of insulin receptor substrate - 1 and of the insulin receptor, increased the antiphosphotyrosine - associated and insulin receptor substrate - 1
associated phosphatidylinositol 3 - kinase activity and stimulated Akt activity.
Antigen - specific enhancement of natural human IgG antibodies to phosphatidylcholine, phosphatidylglycerol,
phosphatidylinositol -4-phosphate, cholesterol, and lipid A by a liposomal vaccine Containing lipid A.Vaccine.
Western blot analyses with phospho - specific antibodies suggested that stretching induces phosphorylation of ERK of the MAP kinase pathway, but did not induce phosphorylation of
phosphatidylinositol 3 - kinase.
Interactome mapping of
the phosphatidylinositol 3 - kinase - mammalian target of rapamycin pathway identifies deformed epidermal autoregulatory factor - 1 as a new glycogen synthase kinase - 3 interactor
Molecular genesis of cutaneous melanoma pathways; rous avian sarcoma homologue (Ras); v - raf murine sarcoma viral oncogene homologue B1 (BRAF); mitogen - activated protein kinase (MEK); extracellular signal - regulated kinase (ERK); microphthalmia transcription factor (Mitf);
phosphatidylinositol - 3 kinase (PI3K); murine v - akt oncogene homologue (Akt).
Research in the Emerling Lab is focused on phosphoinositide signaling, in particular the role of
the phosphatidylinositol -5-phosphate 4 - kinases (PI5P4Ks) in cancer metabolism.
Burke specifically studies the phosphoinositide 3 - kinase and
phosphatidylinositol 4 - kinase families.