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Pyrimidine within Tyrosine Kinase and other (PSTGk, PSTCk, PSTAk) Kinases Produced from MTOR-Fox Binding through Effects of Ser/Thr Phosphorylation Mechanism Play Necessary Rules for Removing Insulin Resistance and Tumors | Abstract
Organic Chemistry: Current Research

Organic Chemistry: Current Research
Open Access

ISSN: 2161-0401

+1-504-608-2390

Abstract

Pyrimidine within Tyrosine Kinase and other (PSTGk, PSTCk, PSTAk) Kinases Produced from MTOR-Fox Binding through Effects of Ser/Thr Phosphorylation Mechanism Play Necessary Rules for Removing Insulin Resistance and Tumors

Ashraf Marzouk El Tantawi*

MTOR genes are originated and activated from ribosomal genes S6K1 and p70S6 with the mitochondrial contributions. mTOR pathway is considered as necessary tools for regulating and activating necessary cellular pathways by which eukcaryotic cells adjust their protein biosynthetic capacity for nutrients needs and availability. The necessary phosphorylation processes on pro-mTOR protein leads to production of four kind of protein kinases for running and regulating most of cellular metabolism and for the blood circulation. the G-protein kinase and GTPase synthesis will contribute most of cellular and genes activities throughout the binding of pro-mTOR with FOX forkhead genes for production of the four kind of protein kinases and for increasing the FOX stabilities, that will lead to sestrin-Leu-1 synthesis, S6K1 genes production, and cholesterol production. During the binding of mTOR with FOX genes, the resynthesis of necessary hydrophobic amino acids will be done with the contribution of mitochondrial enzymes and GTPase, then, the PSTG, PSTC, PSTT and PSTA Protein kinases will be produced with the productions of PTEN protein and S6K1 genes. The mTORC1 will be formed from PSTC protein Kinases for tRNAs, for autophagy productions and for regulating the mTORC2 synthesis.

Published Date: 2021-04-23; Received Date: 2021-04-02

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