Toll-like Receptor-4 Synthesis Regulated by JNK Signaling by Three Glucocorticoids Isoforms, and by Three Interferons Isoforms: Its Advantages in Activities Depending on the Containment from Arg, Proline, and Hydrophobic Amino Acids in its Compositions

Ashraf Marzouk El Tantawi

Abstract


Toll-like receptor-4 (TLR4) synthesis is regulated by JNK signaling, by three glucocorticoids isoforms, and by the three interferons isoforms. It depends on availabilities of LPS & on long fatty acids chains with Arg and proline availabilities for performing and running the mitochondrial oxidative processes for producing fatty-acyl-CoA-synthetase followed by fatty-acyl-CoA-synthase followed by fatty-acyl-CoA-phospholipase productions for linear TLR4 active beta-subunits which will be transformed into TLR4-alpha upon phospholipase effects, which will follow phosphorylation process (alpha-oxidations) for generate guanosine triphosphate cyclohydrolase (GTP-Chase) subunits which supposed to contain specific hydrophobic amino acids including Arg, Tyr, leu, proline, which is the rate-limiting enzyme for tetrahydrobiopterin (BH4) synthesis, which is essential for inducible iNOS from fatty-acyl-CoA-synthase upon the nitric oxide-synthase (NO-S) regulations effects. Proline can accelerate anabolic oxidative processes by OPA1 enzymes and provides site-specific flexibility for collagen synthesis in vivo. It also plays an necessary important role in TLR4 and TGF-gamma/beta/& alpha synthesis and activities, where the presence of proline in IFN-gamma, in TLR4 genes and in IFN-beta will accelerate oxidative OPA1 anabolic processes and direct the flow of biological processes to proliferations of plasma-membranes, collagen synthesis and blood platelets biosynthesis.

Vitamin E & K-dependent protein C are the key components of anticoagulant serine protease. Therefore, vit E and vit k are providing specific advantages to TLR4 synthesis and modulated first in vivo as proper fatty-acyl-CoA-synthetase subunits (gamma-subunits) then modified fatty-acyl-CoA-synthase subunits upon synthase effects on gamma-subunits for producing IL-beta upon which will promote linear TLR4 upon both synthase and phospholipase effects for starting proliferation steps started by catalyzing Arg for producing GTP-Chase and citrulline which the main basis for erythropoietin productions, for plasma membrane synthesis.

Both IFN-beta and glucocorticoid-beta are designed anti-inflammatory subunits depending on each other and on the activities of OPA1-synthase enzyme for producing the long fatty acyl-CoA-synthase (beta-subunit) with specific compositions and sequences from amino acids which can determine their advantages in immunity functions, e.g. their containment of tyr, proline, Arg, gly, where, both glucocorticoid-beta and IFN-beta are able to recover each other in their different tissues.

Keywords: Pro-nutrients-mTOR-FOX, Peptides-kinases, Extracellular-signal-regulated-kinase, TLR4, IL-beta, TGF-beta, IFN-isoforms, BH4, ATPase, mitochondrial-OPA1-membrane


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Copyright (c) 2021 Ashraf Marzouk El Tantawi

Copyright CC BY © European Modern Studies Journal 2017-2021   ISSN 2522-9400

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