| Outline of Final Research Achievements |
The beta3 adrenergic receptor (beta3AR) was analyzed for its impact on overactive bladder, with the purpose of exploring treatment methods. Particularly, attention was focused on the role of adrenaline and nitric oxide (NO) in the relaxation/contraction of the bladder during urinary storage/voiding. NO was found to reduce the metabolic turnover of palmitoylation modification in beta3AR, through the inactivation of DHHC protein, an enzyme responsible for palmitoylation modification, as well as the de-palmitoylation enzyme. Consequently, this led to a decrease in receptor expression on the cytoplasmic membrane of beta3AR and a reduction in downstream cyclic adenosine monophosphate (cAMP) production. It has been discovered that the effects of NO extend beyond vasodilation, impacting various palmitoylation-modified proteins, including human beta3AR.
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