Two SUMO modification sites existed in dopamine receptor D1, the phosphorylation of which, due to SUMO modification, can interact with PP2A, leading to the inhibition of D1 de-phosphorylation and normal function, thus providing new insights for treatment and prevention of hypertension.
A Restriction Fragment Length Polymorphism (RFLP) assay, involving the insertion of a novel Drd I cleavage site in the proline variant revealed a statistically significant over-representation of the cx37*1 allele in association with atherosclerotic plaque-bearing individuals (Odds-ratio for the homozygote = 2.38, Chi2 = 7.693, P = 0.006), in comparison to individuals lacking plaque, irrespective of a history of hypertension.