addition to GTPases, the protein kinase GRK1 also known as rhodopsin kinase (RK) has been shown to undergo farnesylation and carboxyl methylation directed by the carboxyl terminal CVLS CaaX box sequence of the protein. The functional consequence of these post-translational modifications have been shown to play a role in regulating the light-dependent phosphorylation of rhodopsin, a mechanism involved in light adaptation. Inhibitors FTIs can also be used to inhibit farnesylation in parasites such as Trypanosoma brucei and malaria. Parasites seem to be more vulnerable to inhibition of farnesyltransferase than humans are. In some cases, this may be because they lack geranylgeranyltransferase I. Thus, it may be possible for the development of antiparasitic drugs to 'piggyback' on the development of FTIs for cancer research. In addition, FTIs have shown some promise in treating a mouse model of progeria, and in May 2007 a phase II clinical trial using the FTI lonafarnib was started for children with progeria. In signal transduction via G protein, palmitoylation of the α subunit, prenylation of the γ subunit, and myristoylation is involved in tethering the G protein to the inner surface of the plasma membrane so that the G protein can interact with its receptor. Small molecules prenylation Small molecules can also undergo prenylation, such as in the case of prenylflavonoids. Prenylation of a vitamin B2 derivative (flavin mononucleotide) was recently described. Longevity and cardiac effects A 2012 study found that statin treatment increases lifespan and improves cardiac health in Drosophila by decreasing specific protein prenylation. The study concluded, "These data are the most direct evidence to date that decreased protein prenylation can increase cardiac health and lifespan in any metazoan species, and may explain the pleiotropic (non-cholesterol related) health effects of statins." A 2012 clinical trial explored the approach of inhibiting protein prenylation with some degree of success in the treatment of Hutchinson–Gilford progeria syndrome, a multisystem disorder which causes failure to thrive and accelerated atherosclerosis leading to early death. See also Myristoylation Palmitoylation Choroideremia, a genetic disease caused by the loss of REP1, REP2 almost compensates, but cannot rescue the slow onset of blindness References Further reading External links Peripheral membrane proteins Membrane biology Post-translational modification