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

Ashraf Marzouk El Tantawi *
 

1. Hospital Union Hospital, Terra Haute, Indiana. USA

Corresponding Author: Dr. Ashraf Marzouk El Tantawi, Clinical Assistant Professor of Medicine University of Texas Medical Branch, Texas

Copy Right: © 2021 Ashraf Marzouk El Tantawi, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.         

Received Date: September 21, 2021

Published date: October 01, 2021

The Purpose of this study

The roles of S6K1 in ATPase, in GTPase synthesis, and consequently in proliferation including endocytic soluble MHC class II synthesis and functions, that diabetes reflect deficiency in pyrimidines synthesis consequently deficiency in estrogen and reflect androgen synthesis with increasing in consuming in purines (A&G) that lead to decreading in anabolic processes and proliferations.

OPA1-synthetase enzymes are so important for producing amino-acyl-CoA-synthstase (gamma-subunits) which considered as basics for regulating glucocorticoids synthesis, Interferon’s isoforms productions, for reactivating macrophages, for MHC class-I synthesis then consequently for endocytic soluble MHC class II synthesis and their endocytic root functions, and then for cellular proliferation. 

S6K1 consider as protected basic subunits for Interferons (IFNs) isoforms synthesis regulated by pyrimidine-kinases.  Asthma is characterized by Prediabetes and diabetes, that reasons of the occurrence the two diseases (Asthma & diabetes) are same. Estrogen formed from Ser/Thr mTOR FOX signaling pathways for glucocorticoids synthesis Upon OPA1 enzymes effects on estrogen, but the feedback of GC to produce estrogen will be upon ATPase on GCs isoforms.

Abstract

The purines and pyrimidines synthesis in vivo are the main basic processes for all of proper active subunits and active genes biosynthesis and for all cellular biological processes where any delays in their production or deficiency in some of their purines or pyrimidine will lead to symptoms of diseases, whether dangerous or benign. 

Mitoconderial TCA cycles are a regulated metabolite related and depending on FOX genes functions and on ATPase with cox activities on carbohydrate, on lipid, and on proteins pro-nutrients-mTOR molecules for producing first long fatty acids chains and lipo-polysaccharides (LPS molecules ) , where, as FOX genes  produce the four gps of kinases ( PSTCk, PSTTK, PSTGk and PSTA-kinases),  as the mitochondrial enzymes (synthetase, synthase and phospholipase) will start their oxidative processes for modifying those four kinases gps for producing only three fatty acyl-CoA isoforms.

The full releasing of PSTGk and PSTAk gps depending on  FOX functions and on ATPase with COX enzymes for S6K1 peptides synthesis (which are full of purines mainly adenosine nucleotides for ATPase repair ) which will be directed to ribosome granules within cells for further modification efforts by OPA1 enzymes for firstly pyrimidine synthesis then producing gamma-subunits upon Gamma-oxidations by synthetase enzymes , where, I consider that the releasing of PSTGk and PSTAk are the  TCA cycles for producing purines kinases or acyl-CoA-purines, (after mitochondrial OPA1 modification effects), where TCA processed normally related and concluded in the releasing of PSTT-Kinase and PSTC-kinase chains (mTORC1) which are depending on synthetase enzymes for pyrimidines synthesis. S6K1 synthesis and functions can controls tubulin acetylation (due to S6K1 is main regulator active peptides for ribosomal repairs and ATPase productions), hence S6K1 active subunits are contributing to the autophagic flux induced by different stress conditions and in different cells.

mTORC1 is the substrates (the basis for regulating S6K1 peptides productions) of regulating and stimulating ribosomal S6-protein-kinase-1 (S6K1) synthesis through Fox Serine/Threonine signalling activated pathways in response to nutrients and growth factors.

The avaliablities of proline (Pro), Arg, Ser, Thr, Leu, and Tyr amino acids in S6K proper peptides will enhance the proper functions of ATPase and its productions which can prevent cancer, coagulation, prevent platelets aggregation, prevent bones weaknesses and erosion of the vertebrae, and prevent diseases symptoms. Na+, K+-ATPase membrane bonding enzynes (MBE) adopt hypertension, where, The N'A+, K+_ATPase (MBE) functions is stabilizing cellls membranes signals activities and adopt the - ve charges signals transmission that adopt and stabilyzing brain activities.

Estrogen formed from Ser/Thr mTOR Fox signaling pathways for glucocorticoids synthesis (the substrat of GCs synthesis) Upon OPA1 enzymes effects on Estrogen, but the feedback of GCs to produce estrogen will upon ATPase & COX regulations on GCs isoforms.

S6K1 consider as protected basic subunits for Interferons (IFNs) isoforms synthesis regulated by pyrimidine-kinases.  Asthma is characterized by Prediabetes and diabetes, that reasons of occurrence the two diseases are same.

Where, positively Asthma is characterized by diabetes symptoms May in the early days of asthma cannot detected but after early days of diabetes can be detected.

MHC Class-I is fatty-acyl-CoA gamma-subunits (IFN-gamma) for modifying their fatty acyl-CoA-beta (IFN-beta) synthesis to be sit and lie on nucleated cells as MHC class-1 for endocytic MHC class-II production which will promote SIRPα synthesis for TLR4 productions.

Signal regulatory protein α SIRP (SIRP-gamma) is the basic for producing IFN-beta then IFN-alpha which activate TLR4 for Plasma membrane synthesis where through feedback will produce firstly MHC class II (IFN-beta upon synthase beta-oxidation) followed by gamma-oxidation for producing MHC Class-I. SIRP-gamma (IFN-gamma ) productions from myeloid are necessary for acting fast on inflammations and infection-ed  cells for analyzing their contents then bind to resulted peptides for modifying its own sensor subunits for promoting the productions of MHC class-I and SIRP-2-Beta  (IFN-beta) upon regulations effects of OPA1 synthase enzyme which will directed to nucleated cells membranes to sit and lie on as MHC class-I which will  promote the the endocytic soluble MHC class II.

The role of functions of the OPA1 oxidations cycles in producing S6K1 for ATPase for producing and for functioning the fatty-acyl-CoAs for producing NADH and then ATPase.

decreasing or deficiency in S6K1 production will reflect the decreasing in the ATPase which also reflect the decreasing in mitochondrial OPA1-oxidations and decreasing in NAD and FAD that reflect the beginning of many diseases as asthma, diabetes, cancers... etc.

Keywords:

_TCA cycles functions

_S6K1 for ATPase synthesis

_ IFN-isoforms

_TLR4

_MHC-class-I

_MHC-class-II

_Four kinds of proteins kinases groups 

_SIRP-gamma, SIRP-beta & SIRPα

_T-cells

_B-cells

Materials:

_FOX genes, 

_S6K1, ATPase and GTPase

_OPA1 enzymes,

_MTORC1, PS/T-Thymine-K, PS/T-Adenosene-k, PS/T-Guanosine-kinases

_Fatty-acyl-CoA-synthetase,

_Fatty-acyl-CoA-synthase,

_Fatty-acyl-CoA-phospholipase

_N'A, K, ATPase

_Renal proximal tubule epithelia,

_Beta-cells and beta chains

_CD8 T cells

_IFN-gamma, IFN-beta, and IFN-alpha

_diabetes and asthma studies

_MHC Class-I, MHC class II

_Signal proteins

_Tyrosine metabolic pathways

_Arg metabolism and proline synthesis

_mast cells

_Nicotinamide adenine dinucleotide, oxidized form (NAD+).

_T-cells

_B-cells

_TGF-gamma, beta, alpha

_TLR4

_myeloid cells

_SIRP-gamma, SIRP-beta, SIRP-α

_phosphatidic acid (PA)

Methods are results

TCA cycles improves antibody, cytokines and acetylCoA production [1].

Mitoconderial TCA cycles are a regulated metabolite, which considered as a part from FOX genes activities and depending on FOX functions, on ATPase, and on OPA1 enzymes activities on carbohydrate, on lipid, and on proteins nutrient molecules., where, as FOX genes produce the four gps of kinases (PSTCk, PSTTK, PSTGk and PSTA-kinases) as mitochondrial enzymes will start their oxidative effect for modifying those four kinases gps for producing only three fatty acyl-CoA isoforms.

The full releasing of PSTGk and PSTAk gps depending on FOX functions and on ATPase with COX enzymes I considered them as TCA cycles for producing purines kinases or acyl-CoA-purines, which normaly concluded the release of PSTT-Kinase and PSTC-kinase (mTORC1) which are depending on synthetase enzymes for pyrimidines synthesis (cytosine and Thymines) for hydrophobic amino acids [2].

The FOX genes pathways functions and ATPase with COX oxidative processes are for producing the four kinases gps are  firstly regulated by ATPase for producing four kinades gps then followed  by mitochondrial  enzymes effects for producing three fatty-acyl-CoA- isoforms started by OPA1 synthetase enzymes effects  - gamma-oxidation) for producing fatty-acyl-CoA-synthetase (gamma-subunits) , that their proper activities are related to and depending on the presence of purines in specific sequences with pyrimidine for hydrophobic amino acids synthesis where some of those necessary amino acids are :
Alanine amino transferase for Alanine (GCC, GCA, GCG ) {for migrating moleculea and the synthesis of mTORC1 (P-S/T-Cytosine kinases) } , related to Arg (AGA , AGG ) {which is necessary for ATPase and GTPase synthesis and reactivities } , related  to Ser (AGT, AGC ){which is necessary for both cytosine kinases and thymine kinases synthesis } , Thr , leu, {which is so necessary for sestrin synthesis and brain activities } and related to Tyr amino acids synthesis (which considered hydrophobic amino acids and imp for regulating most of active subunits and genes ), where the  purifications and synthesis of purines nucleotides (guanine and adenosine) in FOX pathways is considered as the TCA cycles which is a part from FOX genes activities for producing two kinases adenosine kinases and guanosine kinases which are firstly regulated by ribosomal oxidative (ATPase) process and COX oxidations for analyzing pro-nutrient-TOR for producing the ribosomal polypeptides kinases (or lipo-poly-peptides kinases) which have the  advantages of the Containments of  necessary purines  for the next steps of the mitochondrial OPA1 synthetase effects (gamma-oxidations) for necessary pyrimidine nucleotides synthesis where the cytosines and Thymine synthesis are regulated processes by OPA1-synthetase enzymes for full regulating the pyrimidine synthesis for hydrophobic acids production ( by gamma-oxidation upon synthetase effects ), so I consider that synthetase enzymes is a part from OPA1 sequences that can start adopting and regulate TCA cycles (after the first effect of ATPase) which is a part from FOX genes activities for producing purines kinases which will be joined the pyrimidine production from synthetase effects on lipo-nutrients molecules for hydrophobic acids synthesis whithin the produced kinases chains subunits (eg S6K1, and other cytokines  productions upon the effects of synthetase enzymes). 

TCA cycle metabolites in particular, are centrally important determinants of macrophage metabolic re-programming [3]. 

It has been reported that Metabolism in immune cells is no longer thought of as merely a process for adenosine triphosphate (ATP) production [4], but I reported that ATPase  productions are so necessary for all cells specifically immune cells for activating their ATPase productions for creating their necessary active signals transmission for stimulating other cellular biosynthesis and bio-activities which started by the formation of S6K1 peptides which is regulated by  P-S/T-Adenosine-kinases and by P-S/T-Guanosine-kinases subunits, and by mTORC1 together productions and can be  stored in ribosome as S6K1 which upon phosphorylations  will produce ATPase and GTPase that will be directed for repairing OPA1 inner membrane and then will activate the mitochondrial OPA1 synthetase for gamma-oxidation for producing proper necessary gamma-subunits or fatty-acyl-CoA-gamma for Beta-subunit productions upon the synthase effects through beta-oxidations . Where, the death of living cells started by broken ribosomes or mutated RNAs without repair and without producing ATPase or GTPase that will lead mutations or stopping producing acyl-CoA isoforms that can reflect Brocken pathways in TCA cycles and in FOX activities that will stop releasing PSTGk and PSTAk cytokines upon ATPase and COX enzyme oxidative processes that will lead to cells death or pathogenic symptoms.

Also, not that. Tubulin acetylation which regulated by ATPase plays important role in cellular activities including cell polarities that tubulin acetylation forms ATPase and GTPase and depending on ATPase with GTPase productions that reflect healthy status of living cells. 

S6K1 synthesis and functions can controls tubulin acetylation (due to S6K1 is main regulator active peptides for ribosomal repairs and ATPase productions), hence S6K1 active subunits are contributing to the autophagic flux induced by different stress conditions and in different cells.

During tubulin acetylation, S6K1 contributes to the flux of autophagy induced by different stress conditions and in different cells, where, this effect appears to be independent of the kinase activity of S6K1. [5]

That S6K1 has the basis of the synthesis from the two kinases (PSTAk and PSTGk) with the regulations by mTORC1, where their synthesis produced from TCA cycles which is part from FOX functions. That after the two kinase peptides productions (which depends on ATPase phosphorylation) will be modified by mTORC1 for producing S6K1 that can reflect creations of signals effective transmission which will stimulate gamma-oxidation which proceeded by the effects of OPA1 synthetase for producing amino-acyl-CoA-synthstase (gamma-subunits) with enough energy that simplified in the created active signals which used for migrating the produced subunits and stimulating the beta-oxidations.

The effects of OPA1-synthetase (OP1Stase) will be the results of pyrimidine synthesis including cytosine and active signals transmission which will be used for mTORC1 (PSTCk) subunits productions which will be necessary for regulating the biosynthesis of the S6K1 peptides   , then those S6ks will be  directed for inner cells for repairing and re-activating rRNAs  and for  ATPase and GTPase productions  for  mitochondrial OPA1 membrane repairs (OPA1 inner genes)  and for the production of acyl-CoA isoforms upon OPA1 enzymes effects which started by acyl-CoA-synthetase (gamma-subunits )by gamma-oxidation, which are so necessary for controls tubulin acetylation’s and for regulating axon growth through beta subunits productions by beta-oxidation followed by alpha-oxidations  which produce alpha subunits for axon growth and autophagy biosynthesis .So, the conversion of glutamate to glutamate is imp reversed the acetylated tubulin-NKA complex, and is so imp for proline synthesis regulated by TCA cycles.

After, ATPase Effects started on pro-nutrients-mTOR and the beginning of the formation of S1, 2,.6-Kinases. Which can be considered as  a variety of cytokines with different compositions or as variety of kinases  peptides where their composition is from amino acids differ which their functions of activities depends on their Containment from the purines (qualities and quantity) and their Containment from pyrimidines which started by mTORC1 activities  (PST-Cytosine-kinase, then at mitochondrial-synthetase site effects will continuing the thymine purifications and resynthesis necessary hydrophobic acids) on S6K1 production , then S6ks will be stored in cells and adipose tissues as lipo-S6K1 peptides which also can be considered as lipopeptides kinases or  cytokines with different compositions from. Purines and pyrimidine  which afyer storages will be needed to be modified and reactivated through the mitochondrial OPA1 enzymes oxidations  (due to and during stress and stimulating muscles activities) for reproducing fatty-acyl-CoA-synthetase subunits (gamma oxidations ) which considered as the remaing recovery step for  recreating pyrimidines for hydrophobic acids synthesis and creating the needed active signals transmission enough for binding those active  pyrimidine to original purines in their lipo-peptides chains for amino acids synthesis through producing full fatty-acyl-CoA-synthetase subunits , which will follow the effects of synthase oxidations (beta-oxidation ) for reproducing the needed anti-inflammatory subunits Beta-subunit (fatty-acyl-CoA-synthase) where their composition depending basically on the primary gamma-subunits compositions.

The mammalian target of rapamycin (mTOR) positively regulates axon growth [6],

Where, mTORC1 is the substrates (the basis for regulating S6K1 peptides productions) of regulating and stimulating ribosomal S6-protein-kinase-1 (S6K1) synthesis through Fox Serine/Threonine signalling activated pathways in response to nutrients and growth factors.

And the maintaining of glucose supply for protein synthesis (S6K1) is necessary for central nervous system and for the formation of the three acyl-CoAs (isoforms) for fatty acid synthesis [7]. The maintaining of glucose supply (purines supply) is necessary too for reactivating the long fatty acids chains productions upon ATPase effects and COX effects, and for S6K1 synthesis which necessary for controlling platelet activation and aggregate formation [8].

Maintaining glucose supply(purines supply )are necessary for ATPase reactivation  through regulating S6K  production (with proper composition from hydrophobic amino acids eg of proline, ser, Arg, Leu and tyrosine ) which is necessary for reactivating GTPase synthesis which is necessary for reactivating OPA1 membrane enzymes which are necessary for  ROR-gamma, ROR-beta and ROR-alpha active subunits biosynthesis , for glucocorticoids three isoforms productions, and for the three interferons (IFNs) isoforms productions gamma, beta and alpha respectively).

The availabilities of proline (Pro), Arg, Gly, Asp (GAC), Ser, Thr, Leu, and Tyr amino acids are so necessary for S6K proper peptides which enhance the proper functions of ATPase and OPA1 oxidative processes (Gamma, beta, then Alpha) which can analyze tumors, coagulation, prevent platelets aggregation, prevent bones weaknesses and erosion of the vertebrae, and prevent diseases symptoms. But Asp (GAC) is necessary for deliver its purines A&G by cytosine to endocytic ribosomes (where, Cytosine imp for tRNAs productions and for deliver molecules), where A&G are the only necessary purines for ribosomal repairs, for ATPase, and for GTPase synthesis where the GTPase is so necessary for mitochondrial proper OPA1 inner membrane repairs for generating the OPA1 outer membrane. 

The proper ATPase composition is necessary for amphetamine-based anorectic which necessary to maintain neuronal excitability which can rapidly converted into amphetamine in vivo. Na+, K+-ATPase which is a membrane-bound (MBE) enzyme that can maintain signals activities and maintain Na+, K+-ATPase for brain activities [9]. 

Where, Na+, K+-ATPase (MBE)is afoptong hypertension, where, The N'A, K, ATPase functions is stabilizing cellls membranes signals transmission activities and adopt the -ve charges signals transmission that can adopt and stabilizing brain activities.

Also, Stimulation of Na (+), K (+)-ATPase activity (which basically depending on the S6K1 biosynthesis) increases sodium transport across the renal proximal tubule epithelia,[10].
What is the relation of S6K1 to high blood glucose (hyperglycemia) or low blood glucose (hypoglycemia) and diabetic coma?  We begin that diabetic disease include either hyperglycemia or hypoglycemia but we should not describe diabetes according to hyperglycemic or hypoglycemic but those phenomena reflect the Consumption, cracking and loss of ATPase in biological processes without normal repairs or can be repaired but with mutated characters with sever deficiency in pyrimidine nucleotides in S6K1 peptides which is the basis of ATPase synthesis , that (as I mentioned before) the deficiency in Ser amino acids during FOX functions will lead to decreasing in the PSTTK and in PSTCK kinases and will lead to androgen instead of estrogen that will include mutated S6K1 peptides with deficiency in pyrimidine in their subunits chains that reflect deficiency in hydrophilic acids in S6K1 peptides, that S6K1 will be directed to inner cells for producing mutated ATPase which describe as rich of purines with lacking pyrimidine.

As mutated ATPase started for performing its activities will firstly start to consume its own purines without compensation that will lead to increasing in blood glucose without catalyzing or functioning which describes as hyperglycemia.

But hypoglycemia is the phenomena that describe increasing in mitochondrial oxidative processes with decreasing in ATPase biosynthesis (may at the early stages of diabetic Symptoms), that may at early stages of diabetic diseases there are enough ATPase for performing the catalysing of sugar molecules but without ATPase repairs that later will be turned to hyperglycemia. 

Diabetes is the result of a deficiency in Ser amino acids that reflect deficiency in the formation of the kinase PSTTK and PSTCK (mTORC1), which reflect a decreasing in the formation of pyrimidine nucleotides during FOX activities during pro-nutrients-mTOR metabolic pathways, which leads to the decreaseing in the production of estrogen then will be replaced by androgens, synthesis where androgen describe as rich of purines (Adenosine and Guanosine). 

So during S6K biosynthesis with deficiency in Ser amino acids will produce a mutated S6K1 peptides with rich of purines and deficiency of pyrimidines that when  first regulate ATPase productions will produce mutated ATPase  without normal repair  that when the mutated ATPase began its activities will start to use their Containments from adenosine and guanosine for catalyzing pro-nutrients-mTOR molecules for producing LPS and long fatty acids chains ,that ATPase will spend and consume all of its A&G purines nucleotides  that will be brocken completely without normal repairs with depends on Ser availability  on the production of psttk and PSTCK (mTORC1) during FOX activities, that will not stimulate the mitochondrial enzymes activity , which leads to shivering in the body and may diabetic coma due to the loss of and consuming most of ATPase without normal repairs and recovery , and due to the lack of mitochondrial reactivation. . 

Antibodies are   immunoglobulins proteins which can be classified into ribosomal and non-ribosonal peptides and differentiate according to their amino acids Containments (quality and quantity) , where  non-ribosomal peptides that didn't follow the roots for soluble MHC class II synthesis for running endocytic necessary roots functions (as TLR4 synthesis for Plasma membrane synthesis) , and still not modified by OPA1 enzymes activities   for producing proper active cytokines with proper composition from hydrophobic amino acids. Some antibody consists of four or five polypeptides that each Can described as carry the compositions of one of protein kinases that produced from pro-nutrient-mTOR -FOX Ser/Thr Signaling pathway which produce four types of protein kinases as described before.

Each of those antibody peptides when oxidized by OPA1 enzymes will give more optional for generating the three fatty-acyl-CoA isoforms gamma, beta and alpha subunits, that alpha contain alpha, beta and gamma, but beta contain beta and gamma, but gamma contain only gamma subunits, where  those acyl-CoA isoforms subunits are necessary for regulating macrophages and T-cells biosynthesis   and consequently necessary for myeloid and lymphoid cells activities for proper SIRPα productions for MHC class-I synthesis which promote the endocytic MHC class II synthesis.

Those necessary acyl-CoA three isoforms can be functioned directly by OPA1 regulations for glucocorticoids and for the three interferons isoforms re-synthesis, then for SIRP- which will be for MHC class-1 which regulate endocytic soluble MHC class II synthesis for TLR4 re-synthesis endocytic roots of activities.  insulin has two chains A&B that A and B chains become linked together by two sulfur-sulfur (disulfide) bonds. Pro-insulin, insulin, and C peptide are stored in granules in the beta cells to be released in capillaries [10],

The two A&B chains are considered as two kinases protein one is "A"formed from Ser and the other "B" is formed from Thr amino acids through breaking its nucleotides during and through pro nutrient-mTOR-Fox Ser/Thr Pathways which regulated by ATPase and Cox enzymes. But one of them nearly "B" chain is poor of pyrimidines Containment but rich of purines (that has the ability to recover S6K1 for recovering ATPase and GTPase), while the other chain "A" is rich of pyrimidines (Thymine and Cytosine) were, both subunits chains are bonded with sulfur=sulfur bonds within beta-cells for beta-cells functions and secretion.

Immune consists of two types of lymphocytes: T and B cells, that T cells can produce a large number of cytokines through feedback upon the activity of MHC class-I which include and involve synthetase activities, where B cells require specific differentiations and activation conditions to produce cytokines [11].  the beta cells can only produce only kinds of cytokines (as i refered in previous lines of words) the 1st cytokine is the PS/T-Thymine Kinase and PS/T-Cytosine kinase from "A"chain while B chain produce PS/T-Adenosine kinases and PS/T-Guanosine kinases which can Switching the production of antibody isotypes in B cells, differentiation of helper T cells which regulated by cytokines [ 12].

Cytokines are peptides kinases that formed from Ser/Thr -FOX signaling activities regulated by ATPase and Cox then by OPA1 enzymes functions for the three acyl-CoA isoforms productions.  

B chain is has the function of recover S6Ks peptides production   depending on the availabilities of amino acids composition and their cosequences which can be regulated firstly by ATPase sequences arrangements that are firstly be modified throughout TCA cycles (which is part from FOX and pathways) and through mitochondrial OPA1 enzymes for producing antibodies peptides which can be classified to three types of antibodies depending on their Compositions from amino acids and fatty acids:

1, type AB-gamma

2, type AB-beta

3, type AB-alpha

First AB gamma which include synthetase can analyze and destroy beta cells if their "A" chain is absence (in specific cases depending on their Containment from amino acids and depending on continuing of gamma-oxidations) and hepatic cells , but AB-beta  activate Beta-cells and IFN-beta and can protect hepatic and beta-cells and can increase anti-inflammations processes (through beta-oxidations regularity), but AB-alpha can be started to be activated through AB-beta upon effects of phospholipase for accelerating SIRP a myeloid for MHC class-I productions which produce endocytic MHC class II which is responsible for producing the endocytic TLR4 synthesis that regulate plasma membrane synthesis and run proliferations processes.

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