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.
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
Roles of phosphatidylinositol 3 - kinase and osteopontin in steatosis and aminotransferase release by hepatocytes treated with methionine - choline - deficient medium.
Interestingly, PDGF - BB overexpression by modified hDPSCs enhanced the recruitment of hDPSCs both in vitro and in vivo via the
activation of the phosphatidylinositol 3 kinase (PI3K) / Akt signaling pathway and, in combination with secreted vascular endothelial growth factor (VEGF), enhanced in vitro angiogenesis.
In turn it induces the cleavage
of phosphatidylinositol - 4, 5 - diphosphate (PIP2) to the production of two second messengers, inositol 1,4,5 - triphosphate (IP3) and diacyl glycerol (DAG)[41].
Inhibitors (LY294002, wortmannin, and deguelin)
of phosphatidylinositol 3 - kinases (PI3K) and AKT, but not inhibitors of MEK1 / 2, JNK, and p38 - MAPK abolished the ActD - induced p53 expression in diverse cell types.