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RyR2 Serine-2030 PKA Site Governs Ca 2+ Release Termination and Ca 2+ Alternans.

Jinhong WeiWenting GuoRuiwu WangJohn Paul EstilloreDarrell BelkeYong-Xiang ChenAlexander VallmitjanaRaul BenitezLeif Hove-MadsenS R Wayne Chen
Published in: Circulation research (2022)
transient recovery in intact working hearts, whereas CaM-wild-type exerted an opposite effect. The impact of isoproterenol was partially and fully reversed by the PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide and the CaMKII inhibitor N-[2-[N-(4-chlorocinnamyl)-N-methylaminomethyl]phenyl]-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamide individually and together, respectively. S2030L abolished the impact of CaM-wild-type, CaM-M, and N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide-sensitive component, but not the N-[2-[N-(4-chlorocinnamyl)-N-methylaminomethyl]phenyl]-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamide-sensitive component, of isoproterenol.
Keyphrases
  • wild type
  • protein kinase
  • ionic liquid
  • cerebral ischemia
  • blood brain barrier
  • brain injury