An In-Depth Study of TCA cycles, OPA1, S6K1, ATPase, TLR4, MHC-class-I, GCs, and IFNs Bio-Synthesis, and Their Roles of Deficiency in Diabetes, Asthma, Cancer, etc and the NAD Roles in Their Activities

Abstract

The roles of S6K1 is 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 ribosimes. OPA1-synthetase enzymes are important for producing amino-acyl-CoA-synthetase (gamma-subunits) which regulate glucocorticoids synthesis, and Interferons isoforms productions, for reactivating macrophages, and MHC class-I which redulate endocytic soluble MHC class II synthesis which regulate both SIRPα1 and TLR4 productions for cellular proliferation.

S6K1 consider as protected basic subunits for Interferons (IFNs) isoforms synthesis which regulated by pyrimidine-kinases (PS/T-Cytosine Kinase & PS/T-Thymine Kinase) . Asthma is characterized by Prediabetes and diabetes, that the reasons of occurrence the two diseases (Asthma & diabetes) are deficiency in Ser amino acids and consequently deficiency in pyrimidine kinases lead to increasing in Androgen production and deficiency in Estrogen biosynthesis. Estrogen formed from Ser/Thr mTOR FOX phosphorylations signaling pathways for glucocorticoids synthesis regulated by OPA1 enzymes effects , 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 and S6K1 productions.