嘧啶型TAT TAC激酶通过Ang2-AT2合成和抗炎生长促进B-Arrestins和Rac1心肌收缩和Gpcrs比值

Ashraf Marzouk El Tantawi
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引用次数: 0

摘要

孤儿核途径(由嘧啶TAT和TAC激酶以及OPA1酶调节)在合成酶的作用下产生β亚基(fatty Acyl-COAbeta),合成酶调节B-arrestins合成,采用ACE从Ang1-AT1合成Ang2-AT2(采用GPCRs比例)。合成酶和嘧啶激酶的抑制反映了酰基辅酶a - β合成的抑制,随后胆固醇和长脂肪链的积累与k和Na盐的高亲和力结合,可以沉淀并引起脂肪毒性。b -阻滞素在抑制g蛋白偶联受体(gpcr)的积累中发挥着良好的作用,通过其通过ACE激活Ang1-AT1合成Ang2-AT2来阻止其增加。
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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-COAbeta) 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.
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