We hypothesize that secreted diglucosyl-diacylglycerol blocks host binding sites, thereby preventing bacterial adhesion.
2
This was accompanied by a significant increase in diacylglycerol labelling.
3
Affinity was much reduced for 3-phosphorylated inositides while no binding of diacylglycerol was detected.
4
T cells rely on diacylglycerol (DAG) to carry out their functions.
5
This effect was reproduced by exogenous diacylglycerol, but not by a cell-permeable analog of ceramide.
6
This was paralleled by a severalfold amplification of diacylglycerol formation and sustained elevation of cytosolic calcium.
7
This LPP1 effect was upstream of PLD activation in addition to the possible metabolism of phosphatidate to diacylglycerol.
8
Indeed, serum withdrawal resulted in 3-4-fold elevation in endogenous diacylglycerol levels.
9
Naringenin-fed mice exhibited elevated locomotor activity monitored by infrared beam breaks, maintained muscle mass and reduced muscle diacylglycerol content.
10
Thus, the combination of ceramide and diacylglycerol recapitulated the complex effects of serum withdrawal on cell cycle arrest and apoptosis.
11
Generation of diacylglycerol within the nucleus is believed to recruit protein kinase C to the nucleus to phosphorylate intranuclear proteins.
12
Activity of protein kinase C depends on the interaction with polar head-groups of two membrane lipids, i.e., phosphatidylserine and diacylglycerol.
13
We have previously demonstrated that activation of proliferation leads to an increase in the production of nuclear diacylglycerol (DAG).
14
Protein kinase C has been in the spotlight since the discovery two decades ago that it is activated by the lipid second messenger diacylglycerol.
15
Our data show that the levels of diacylglycerol in lavage fluid relative to affected bronchus are elevated in 56% of all the patients examined.
16
Instead, oleate, one of the most common fatty acids in triglycerides, enhances platelet-derived growth factor-BB-mediated proliferation and oleate-containing 1,2-diacylglycerol formation in smooth muscle cells.