Deletion of diacylglycerol kinase ε confers susceptibility to obesity via reduced lipolytic activity in murine adipocytes.

Lipid metabolism is closely involved with signal transduction and energy homeostasis. Excess calorie intake causes abnormal lipid metabolism, promoting obesity and insulin resistance. Diacylglycerol (DG) represents not only a lipidic second messenger but also an intermediate metabolite for triglyceride metabolism in the endoplasmic reticulum (ER).

Diverse Functions of Plasma PAF-AH in Tumorigenesis.

This chapter is focused on the role of the plasma form of platelet-activating factor-acetylhydrolase (PAF-AH), heretofore referred to as PAF-AH, in tumorigenic responses. Biochemical and other properties of this enzyme were discussed in detail in chapter "Plasma PAF-AH (PLA2G7): Biochemical Properties, Association with LDLs and HDLs, and Regulation of Expression" by Stafforini and in other chapters. Although phospholipases tend not to be drivers of tumorigenesis themselves, these enzymes and the lipid mediators whose levels they regulate interact with a variety of oncogenes and tumor suppressors [1].

Plasma PAF-AH (PLA2G7): Biochemical Properties, Association with LDLs and HDLs, and Regulation of Expression.

This chapter is focused on the plasma form of PAF-acetylhydrolase (PAF-AH), a lipoprotein-bound, calcium-independent phospholipase A2 activity also referred to as lipoprotein-associated phospholipase A2 and PLA2G7. PAF-AH catalyzes the removal of the acyl group at the sn-2 position of PAF and truncated phospholipids generated in settings of inflammation and oxidant stress. Here, I discuss current knowledge related to the structural features of this enzyme, including the molecular basis for association with lipoproteins and susceptibility to oxidative inactivation.

Designing a broad-spectrum integrative approach for cancer prevention and treatment.

Targeted therapies and the consequent adoption of "personalized" oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.