Pyrimidine TAT TAC Kinases Promote B-Arrestins and Rac1 for Adopting Myocardial Constrictions and Gpcrs Ratio by Ang2-AT2 Synthesis and Anti-Inflammatory Growth

The orphan nuclear pathway (regulated by pyrimidine TAT and TAC kinases and OPA1 enzymes) has the roles of producing the Beta-subunit (fatty Acyl-COA-beta) upon the effects of synthase which regulate B-arrestins synthesis for adopting ACE for Ang2-AT2 synthesis from Ang1-AT1 (that adopt GPCRs ratio) . The inhibition in synthase and in pyrimidines kinases will reflect Inhibition in Acyl-COA-beta synthesis followed by cholesterol and long fatty chains accumulations with high affinity to bind with k and Na salts that can precipitated and cause lipotoxicity. B-arrestins play a well established role in the dampening of G-protein coupled receptors (GPCRs) accumulation, that prevent their increasing through its adopting to ACE for activating Ang2-AT2 synthesis from Ang1-AT1. The absence of pyrimidine kinases or Ser and Leu with availability of purines kinases produced from Thr phosphorylation can convert the agonist characters of MR to antagonist due to decreasing in adopting MR functions (decreasing in building proper promoters in the active MR molecules). The Glucocorticoid-beta and Estrogen Receptors are so important for producing B-arrestin in Myocardial layer for adopting ACE which placed particularly on ECs for adopting Ang2-AT2 synthesis (adopt Ang1-AT1 ratio to prevent accumulation of GPCRs ), and activate the regulated VEGF-A “regulated basically pyrimidine kinases “.