ATPase Effects on Pro-Nutrients-mTOR Release Long Fatty Acids Chains which Under Mitochondrial Phospholipase, Synthase, & Synthetase Effects form Three ROR-Alpha, Beta, Gamma Isoforms
Authors:   Biomedical Molecular Studies, Cairo Egypt, AM El Tantawi 
Published: June 2021

RORs isoforms are a metabolic strong regulators have their own functions in the lipid metabolism and in genes, subunits, and hormones reproductions, where during their necessary metabolic activities on lipid metabolism with the effects Mitochondrial enzymes on lipid molecules the acyl-CoA-synthase (RORbeta), acyl-CoA-phospholipase (ROR-alpha), and acyl-CoA-synthetase (RORgama) will be synthesised and released for running the lipid metabolic pathways. Where the RORs isoforms functions are strongly linked to FOX forkhead genes and strongly depending on mitochondrial anabolic active enzymes activities (phospholipase, synthase, synthetase), and are having a strong regulations by mitochondrial OPA1 membrane which act on long fatty acids molecules for releasing the three enzymatic acyl-CoA active molecules for the cholesterol productn, for TNF-a with TXA2 alpha subunits productions, for sestrin-Leu 1 synthesis, for prostaglandins synthesis which reflect the strengthen of ROR-beta with ROR-alpha activities, for S6K1 production, and for estrogen & insulin growth and their ratio biosynthesis. When lipid associated with absorbed nutrient molecules (pro-lipo-mTOR) will be firstly affect by ATPase and by Cox2 for releasing long fatty acids molecules and will be directed to FOX forkhead and to ROR genes, where first the ATPase and COX-2 will act on lipid molecules for releasing long fatty acids molecules then the mitochondrial anabolic enzymes effects will act fatty acids molecules for releasing the acyl-CoA-phospholipase (ROR alpha isoforms), acyl-CoAsynthase (ROR-beta), and acyl-CoA synthetase (ROR-gama isoforms), where all RORs isoforms are having the same molecular structure but differ only in their terminals. The decreasing in mitochondrial synthetase enzyme will reflect inhibition or decreasing in acyl-CoA-synthetase enzymatic molecules (ROR-gama) synthesis which adopted for carbohydrate metabolic cycles and the ratio of pyrimidine in biological molecules, that can reflect decreasing in the pyrimidine synthesis from purines which will lead to decreasing in hormone biosynthesis, and sestrin biosynthesis, and decreasing in RORs isoforms stabilities and activities, which can reflect decreasing in FOX genes stabilities, and decreasing in Thymine kinases molecules activities which consequently lead to inhibition or decreasing in cholesterol biosynthesis, and in estrogen or insulin hormones biosynthesis pathways. Long-fatty acyl-CoAs are produced due to the effects of mitochondrial anabolic enzymes on the long fatty acids molecules which produced from the effects of ATPase and mitochondrial COX-2 on the lipid molecules, which considered as necessary anabolic regulatory and intermediates molecules in lipid metabolic pathways and in the active kinases molecules resynthesis during the binding of Pro-nutrients-mTOR molecules. Following the long fatty acids formation by the effects of ribosomal ATPase is the effect of mitochondrial OPA1 membrane activities for producing its necessary anabolic mitochondrial enzymes (phospholipase, synthase, and synthetase) for producing the three RORs isoforms active enzymatic molecules acyl-CoA-phospholipase (ROR-alpha), acyl-CoA synthase (ROR-beta), acyl- CoA synthetase (ROR gama). The RORs isoforms consedered as three structures of RORs isoforms, each isoform bind to one of the anabolic mitochondrial enzymes (synthase, synthetase, and phospholipase enzymes)to form its own ROR-isoforms, and each of RORs isoforms has its own specific functions and pathological pathways but is contributing with others RORs-isoforms for running and completing their specific biosynthesis pathways during lipids metabolism. Those RORs (the enzymatic acyl-CoA) isoforms molecules are having same molecular structures but differs only in their terminal amino acids, and are incorporated into acylated proteins and complex active fatty molecules like triacylglycerol, phospholipids, and cholesterol esters for activating the brain metabolic processes, for the liver metabolic activities, and for the strengthen of immune efficiency through TNF-Alpha and TXA2 subunits productions by the acyl-CoA-synthase (ROR beta isoforms ) and for sestrin-Leu biosynthesis through the regulation of acyl-CoA-synthetase (ROR gama isoforms). The synthesis of each of acyl-CoA isoform firstly by the effects of ATPase and COX-2 on lipid molecules followed by the mitochondrial OPA1 activaties for releasing its active enzymatic acyl-CoA isoforms during lipid metabolism. As ribosomal ATPase act on lipo-mTOR protein will release long fatty acids molecules then will be followed by mitochondrial effects on long Fatty molecules for producing enzymatic acyl-CoAs (RORs) isoforms. Where acyl-CoA isoforms molecules will be binded to whether synthetase, phospholipase, or to synthases enzymes as intermediates for brain activities, for liver functions etc., depending on the type of signals activities received from brain and from cells to form RORs isoforms. The mitochondrial enzymes effects are necessary (anabolic snd antiinflammatory enzymes) for RORs isoforms biosynthesis, and are considered as anti-inflammatory regulating enzymes that synthase and synthetase are so necessary for TNF-a and for thromboxane-A (TXA2) biosynthesis, and regulate the releasing of the active four kind of kinases proteins during the FOX binding activities, and act as mediators for anti inflammations pathways as for prostaglandins productions, and are acting releasing the ROR-alpha isoforms which are active isoforms for phospholipid membranes and for antigen biosynthesis. Liver X Receptors (LXRs) are nuclear receptors, that LXRs were originally considered as ‘orphan’ nuclear receptors, and it’s origin depend on the synthesis of acyl-CoA phospholipase isoforms which is the basic of liver cells phospho-lipo-membrane. However, those receptors were ‘adopted’ for running lipid metabolism, cholesterol synthesis, and phospholipid membranes which act as so imp biological filter for and from nucleus. The phospholipid membranes formed from acyl-CoA-phospholipase (RORalpha) isoforms functions, where phospholipid are imp molecules for skeletal muscle development, for photoreceptor development and for liver activities. IFN gamma depending on biosynthesis effects of synthetase enzymes on long fatty acids chains for producing fatty acyl-CoAs synthetase which act as a protective IFN-gamma in regulating the retinal hydrations. PLC-gamma1 is implicated in a variety of cellular signalings and processes including mitogenesis and calcium entry. The Nerve growth factor is a neurotrophic factor and neuropeptide primarily involved in the regulation of growth, maintenance, and proliferation that has imp roles in carbohydrate biosynthesis for maintaining the necessary balances of purines related to pyrimidine nucleotides through the pyrimidines synthesis where their results will feed the sensor nerve and neuronal hyper reactivity for nerve activities. The effects of synthase and phospholipase on the productions of RORs beta and alpha isoforms respectively are cooperating together for running so imp osteogenic repressor in regulating bone formation and in new blood cells synthesis with their effective phospholipid membranes, and are imp for TNF-a and TXA2 alpha subunits productions, where PSTC-kinases (mTORC1) and thromboxane-A2 can used for the autophagy reactivities and biosynthesis. Heart failure is associated with decreased myocardial fatty acid metabolic pathways and decreasing in fatty acids functioning and oxidation capacity and has been likened to energy starvation. As the adenosine metabolism in tissues have been consumed due to extra ATPase and COX-2 activities as energy utilization will increased from breaking and analyzing genes and fatty acyl-CoA molecules and from pyrimidine molecules lead to precipitation of ub normal molecules which can block blood fluidity in arteries and veins leads to decreasing in heart muscle lead to heart failure.