Pyrimidine TAT TAC Kinases Promote B-Arrestins and Rac1 for Adopting Myocardial Constrictions and Gpcrs Ratio by Ang2-AT2 Synthesis and Anti-Inflammatory Growth
{"title":"Pyrimidine TAT TAC Kinases Promote B-Arrestins and Rac1 for Adopting Myocardial Constrictions and Gpcrs Ratio by Ang2-AT2 Synthesis and Anti-Inflammatory Growth","authors":"Ashraf Marzouk El Tantawi","doi":"10.47363/jjcmr/2022(2)141","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":415591,"journal":{"name":"Japan Journal of Clinical & Medical Research","volume":"58 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japan Journal of Clinical & Medical Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.47363/jjcmr/2022(2)141","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.