High impact information on tetradecyl ethanoate

• Constitutive expression of PAC1 in vivo leads to inhibition of MAP kinase activity normally stimulated by epidermal growth factor, phorbol myristyl acetate, or T-cell receptor crosslinking [1].
• We show that the proapoptotic activity of alpha-TOS in hematopoietic and cancer cell lines involves inhibition of protein kinase C (PKC), since phorbol myristyl acetate prevented alpha-TOS-triggered apoptosis [2].
• A decreased level of IL-2 was produced by GFP+ cells after phorbyl myristyl acetate and ionomycin stimulation [3].
• Autocrine regulation of apoptosis was demonstrated by increased FasL activity after stimulation of GFP- cells with anti-CD3, phorbyl myristyl acetate plus ionomycin, or Con A [3].
• By using immunogold labeling at the electron microscopy level, we demonstrated that phorbol myristyl acetate induced the redistribution of SGLT1 protein from intracellular sites to the plasma membrane [4].

Biological context of tetradecyl ethanoate

• Phorbol myristyl acetate induced phosphorylation of C-CAM-S in transfected CHO cells [5].
• DAG and its analogues phorbol myristyl acetate and 1-oleoyl-2-acetylglycerol did not affect membrane potential either when applied by perfusion or when injected [6].

Anatomical context of tetradecyl ethanoate

• Adhesion assays were performed with HAEC stimulated with interleukin (IL)-1 beta or U937 cells activated with phorbol myristyl acetate; ROS were measured after challenging HAEC with IL-1 beta or hydrogen peroxide [7].

Gene context of tetradecyl ethanoate

• Release was Ca2+ dependent and stimulated by either phorbol myristyl acetate (a protein kinase-C activator) or NaF (a G-protein activator) [8].

References