Abstract

RORs isoforms are so active biological molecules in lipid metabolism and in fat biosynthesis, that strongly dependent on and regulated by OPA1 mitochondrial genes and its active mitochondrial enzymes where each of mitochondrial enzyme (phospholipase, synthase, and synthetase) is responsible for its own ROR isoform {phospholipase responsible for ROR-alpha synthesis, synthase responsible for ROR-beta synthesis, and synthetase responsible for ROR-gamma synthesis} for acting and functioning the long fatty acids molecules “which produced from the effects of ATPase and COX enzyme on lipid molecules which accompanied and associated with absorbed nutrient molecules (pro-lipo-nutrient -mTOR molecules)”, and then will follow its own pathway in fatty and amino acids biosynthesis, in active anti-inflammations biosynthesis, and then will follow its own functions in original cells proliferations. Where, Lipid molecules+ATPase+COX enzymes ¬¬>long Fatty acids molecules +mitochondrial active phospholipase + ribosomal ATPase (in a control limit) ¬-> long Fatty acid-acyl-CoA phospholipase (which is ROR-alpha active isoforms), ¬¬>>Fatty acyl-CoAsynthase which is ROR beta active genes, And ¬¬>> fatty acyl-CoA-synthetase (which is ROR-gama isoforms) then both ROR-alpha and ROR-gama +AMP ¬> isopentanyl PP+ Leu (or Meth) amino acids ¬> leu-pentapeptides (or Meth-pentapeptides) active molecules for activating enkephalin tissue in brain. ATPase and COX enzymes are responsible for acting on lipid associated with nutrients-mTOR for producing long fatty acids molecules which will be affected by mitochondrial phospholipase, synthase and synthetase to form ROR-alpha, ROR-beta and ROR-gamma respectively.

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