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

E. Am
{"title":"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":"E. Am","doi":"10.26420/austinjmedoncol.2021.1062","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":8626,"journal":{"name":"Austin journal of medical oncology","volume":"39 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Austin journal of medical oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26420/austinjmedoncol.2021.1062","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

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.
atp酶对原营养物- mtor释放长脂肪酸链的影响,在线粒体磷脂酶、合成酶和合成酶的作用下形成三种ror - α、β、γ亚型
RORs亚型是一种代谢强调节因子,在脂质代谢和基因、亚基和激素复制中具有自己的功能,在脂质代谢中,线粒体酶对脂质分子的作用,在脂质代谢中,酰基辅酶a合成酶(rorβ)、酰基辅酶a磷脂酶(rorα)和酰基辅酶a合成酶(RORgama)将被合成和释放,以运行脂质代谢途径。其中RORs同工异构体的功能与FOX叉头基因密切相关,并且强烈依赖于线粒体合成代谢活性酶(磷脂酶、合成酶、合成酶)的活性,并且受到线粒体OPA1膜的强烈调控,后者作用于长脂肪酸分子,释放三种酶促酰基辅酶a活性分子,用于胆固醇的产生,用于具有TXA2 α亚基的TNF-a的产生,用于凝血素-亮氨酸1的合成。前列腺素的合成,反映了ror - β与ror - α活性的增强;S6K1的产生;雌激素和胰岛素的生长及其比例生物合成。当与被吸收的营养分子相关的脂质(前脂质- mtor)首先受到ATPase和Cox2的影响,释放长脂肪酸分子,并被引导到FOX叉头和ROR基因,其中ATPase和COX-2首先作用于脂质分子释放长脂肪酸分子,然后线粒体合成代谢酶作用于脂肪酸分子释放酰基辅酶a -磷脂酶(ROR α亚型),酰基辅酶合成酶(ROR β),酰基辅酶a合成酶(RORs - γ异构体),其中所有的RORs异构体具有相同的分子结构,只是末端不同。线粒体合成酶的减少反映了用于碳水化合物代谢循环和生物分子中嘧啶比例的酰基辅酶a合成酶酶分子(ror - γ)合成的抑制或减少,反映了嘌呤合成嘧啶的减少,从而导致激素生物合成和半胱氨酸生物合成的减少,RORs同工异构体的稳定性和活性下降。这可以反映出FOX基因稳定性的降低,胸腺嘧啶激酶分子活性的降低,从而导致胆固醇生物合成以及雌激素或胰岛素激素生物合成途径的抑制或减少。长脂肪酰基辅酶a的产生是由于线粒体合成代谢酶对长脂肪酸分子的作用而产生的,长脂肪酸分子是atp酶和线粒体COX-2对脂质分子的作用产生的,被认为是脂质代谢途径中必要的合成代谢调节和中间分子,是Pro-nutrients-mTOR分子结合过程中活性激酶分子再合成的中间分子。在核糖体atp酶的作用下形成长脂肪酸后,线粒体OPA1膜活性产生其必需的合成代谢线粒体酶(磷脂酶、合成酶和合成酶),以产生三种RORs同工型活性酶分子酰基辅酶a -磷脂酶(ROR- α)、酰基辅酶a合成酶(ROR- β)、酰基辅酶a合成酶(ROR- γ)。RORs异构体被认为是RORs异构体的三种结构,每个异构体与一种合成代谢线粒体酶(合成酶、合成酶和磷脂酶)结合形成自己的RORs异构体,每个RORs异构体都有自己特定的功能和病理途径,但在脂质代谢过程中与其他RORs异构体一起运行和完成其特定的生物合成途径。这些RORs(酶促酰基辅酶a)同工异构体分子具有相同的分子结构,但仅在末端氨基酸上有所不同,并被纳入酰基化蛋白质和复杂的活性脂肪分子中,如三酰基甘油,磷脂和胆固醇酯,以激活大脑代谢过程,促进肝脏代谢活动,以及通过酰基辅酶a合成酶(ROR β亚型)产生tnf - α和TXA2亚基来增强免疫效率,以及通过调节酰基辅酶a合成酶(ROR γ亚型)来进行凝血素-亮氨酸生物合成。每种酰基辅酶a异构体的合成首先通过atp酶和COX-2对脂质分子的作用,然后在脂质代谢过程中线粒体OPA1激活释放其活性酶酰基辅酶a异构体。由于核糖体atp酶作用于脂肪- mtor蛋白会释放长脂肪酸分子,随后线粒体作用于长脂肪分子产生酶酰基辅酶a (RORs)同工型。其中酰基辅酶a异构体分子将结合到合成酶、磷脂酶或合成酶作为脑活动、肝功能等的中间体,这取决于从脑和细胞接收到的信号活动的类型,形成RORs异构体。
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