An In-Depth Study in TCA Cycles, OPA1 Enzymes Functions, S6K1, Bio-Synthesis, and Their Roles in ATPase, IFNs, GCs, MHC-Class-I, MHC-Class-II, SIRPα1 and TLR4 Biosynthesis

  • Ashraf Marzouk El Tantawi
Keywords: TCA cycles functions, S6K1 for ATPase synthesis, IFN-isoforms, TLR4, MHC-class-I, MHC-class-II, four kinds of proteins kinases groups, SIRP-gamma, SIRP-beta & SIRPα, T-cells, B-cells


The roles of S6K1 are regulating ATPase and GTPase synthesis, and consequently the endocytic proliferations including endocytic soluble MHC class II synthesis which regulate both SIRPα1 and TLR4 synthesis, where diabetes reflect deficiency in Ser amino acids that reflect deficiency in pyrimidines synthesis consequently deficiency in Estrogen and reflect increasing in androgen synthesis with increasing in consuming in purines (A&G) that lead to decreasing in anabolic processes which depends on presence of adenosine and guanosine stored in ribosomes. OPA1-synthetase enzymes are necessary for producing amino-acyl-CoA-synthetase (gamma-subunits) which regulate glucocorticoids synthesis, and Interferons isoforms productions, for reactivating macrophages, and MHC class-I which regulate the endocytic soluble MHC class II synthesis which regulate both SIRPα1 and TLR4 productions for cellular proliferation. S6K1 promote ATPase synthesis for regulating ribosome, ATPase, and Interferons (IFNs) isoforms synthesis, where S6K regulated by purine-kinases (PS/T Adenosine Kinase & PS/T-Guanosine Kinase) productions from Ser /Thr phosphorylation signaling pathway. Asthma is characterized by prediabetes and diabetes, that the reasons of causing the two diseases (asthma & diabetes) are the deficiency in Ser amino acids and consequently deficiency in pyrimidine kinases productions leading to increasing in Androgen production but deficiency in Estrogen biosynthesis. Estrogen formed from Ser/Thr mTOR FOX phosphorylations signaling pathways for glucocorticoids synthesis regulated and modified by OPA1 enzymes effects for producing acyl-CoA-glucocorticoids isoforms, but the feedback of GC to produce estrogen will be upon ATPase & synthetase enzymes on GCs isoforms followed by Ser /Thr phosphorylation signaling pathway which will promote both Estrogen, protein kinases, and S6K1 productions.