Журнал диагностики рака

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Mitochondrial Inner Optic Atrophy 1 (OPA1) Gene is Necessary for Regulating and Activating Lysosome, Related Orphan Receptor A (ROR- α) genes, and APOL1 Gene Involved in Autophagy Cells for Antiinflammation Processes, Where ROR-α Genes Stored as Lysosomal Security Granules Within Autophagy Cells.

Tumor Necrosis Factor alpha (TNF-α) subunits deficiency or the involvement in will lead to Sickle Cell Disease (SCD) which marked by a phenotypic variability and inflammation plays the major role in SCD pathophysiology, which linked strongly to ROR-α1 genes expression and functions, and also linked to TNF-α subunits expressions and. Activities, where TNF-α subunits are so essential for anti-inflammation processes and linked to ROR-α genes activities and functions, and necessary for regulation of bone homeostasis in several chronic immune and inflammatory joints and tissues diseases. The inhibition of TNFα due to inhibition or variations in ROR-α genes lead d to significant inflammations improvements involved in SCD pathophysiology, and also will lead to increasing in Nuclear factor-κB pathways (NFκB) catabolic pathways and any remaining of TNF-α will be involved in the NF-κB signaling pathway due to inhibition in their mitochondrial activities. The inhibition or deficiency in presence of Thymine in the Related Orphan Receptor-A (RORA) genes can reflect deficiency in mitochondrial synthetase enzyme (where mitochondrial OPA1 gene depending on ribosomal genes activities ), that’ll lead to down activities in ROR-α genes functions, and reductions in TNF-α, TXA2, and in VEGF-A subunits. Lysosome and ROR-α genes are having so necessary functions of preventing G-protein aggregates associated with neuropathies, and preventing blood platelets aggregations depending on mitochondrial activities through producing its active inflammatory enzymes for acting on any toxic inflammation or on any aggregation for producing the active TXA2 subunits which through feedback will reforme VEGF-A alpha subunits where can be stored in or as lysosomal secretory granules. ROR-α gene is so necessary for anti inflammations where ROR alpha active gene depending on mitochondrial anti inflammatory enzymes (synthase, phospholipase, Cox2 enzymes) and regulated by mitochondrial inner membrane OPA1 genes activities which are strongly repaired by acyl-CoA:l-acyl-sn-glycero-3-phosphocholine O-acyltransferase. Where acyl-CoA:l-acyl-sn-glycero-3-phosphocholine O-acyltransferase enzyme is so necessary for re-activating brain acetylcholine and for mitochondrial inner membrane repair and protect liver from fibrosis. Reductions in mitochondrial activities will lead to reductions in ROR-α genes activities and consequently will lead to reductions in TNF-alpha and in CYP7A genes expression and functions (which are locally produced in brain, and in liver ), and will lead to a hepatopathy, encephalopathy, a variants of Syndromic Intellectual Disability. Where, ROR-α genes are necessary for CYP7A genes productions and activities which are necessary for the Conversions of both cholesterol and 27-hydroxycholesterol into bile acids. ROR-α genes considered is imp for regulating anti-inflammations procedures and necessary for controlling the conversion of cholesterol and 27-hydroxycholesterol into bile acids and are so essential for liver protections and are so necessary for protection from sickle cells diseases. Where during autophagy activities which contain APOL1 protein (lipoproteins) will need phospholipase enzyme for activating APOL1 gene involved in autophagy cells which expressed from mitochondrial membrane for activating the autophagic APOL1 gene for expressing ROR-α genes from the autophagy cells for fast acting on inflammations, where that previous fact reveal “and I consider it as” that ROR-α genes are stored within autophagy cells as active lysosomal security granules for fast acting on tumors and on inflammations molecules which are involved with the pathogenesis of various disorders, including cancer, neurodegeneration, and inflammatory diseases. But in the case of deficiency of mitochondrial activities or in case of inhibitions of phospholipase enzyme expressed from mitochondrial membrane will lead to un activating APOL1 genes lead to inhibition in releasing ROR-α gene from autophagy cells and then involved in tumor contents and in interstitium fluid as inactive molecules.