In collaboration with the study group of Susan Taylor, PhD, professor of pharmacology at UC San Diego School of Medicine, Newton and experts took another appearance at how exactly to connect the right parts, or domains, of the enzyme. They came up with a different framework and tested it utilizing a sophisticated cellular imaging strategy to visualize whether PKC was correctly loaded together or not. The researchers discovered that PKC's calcium-sensing domain interacts using its own tail and enzymatic domain , locking the enzyme in an inactive pose. PKC starts to activate when calcium triggers the bridging of the C2 domain to the cell membrane, starting the enzyme for activity thus.Holme, Ph.D., David Kallend, M.B., B.S., Lawrence A. Leiter, M.D., Eran Leitersdorf, M.D., John J.V. McMurray, M.D., Hardi Mundl, M.D., Stephen J. Nicholls, M.B., B.S., Ph.D., Prediman K. Shah, M.D., Jean-Claude Tardif, M.D., and R. Scott Wright, M.D. For the dal-OUTCOMES Investigators: Ramifications of Dalcetrapib in Individuals with a Recent Acute Coronary Syndrome High-density lipoproteins participate in the process of cellular cholesterol efflux and could have additional protective effects against atherothrombosis.1 An inverse association between degrees of HDL cholesterol and incident events of coronary heart disease has been shown in observational studies2,3 and persists generally in most post hoc analyses and meta-analyses of trials of statin therapy for patients with cardiovascular risk factors, chronic coronary disease, or recent acute coronary syndrome.4-10 However, it remains uncertain whether pharmacologic intervention that raises HDL cholesterol levels outcomes in reduced cardiovascular risk.11-16 Moreover, changes in HDL cholesterol levels might not reflect changes in the physiologic functions of HDLs.17 Cholesteryl ester transfer proteins mediates the transfer of cholesteryl ester from HDLs to atherogenic lipoprotein particles containing apolipoprotein B, such as low-density lipoprotein .