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^*

*Corresponding Author: Dr. Ashraf Marzouk El Tantawi Biomedical molecular studies. Cancer and viral infections. Canada, Toronto, Goldwin Av. Egypt, Giza, Abd elmonem R.

Received Date:  February 24, 2021

Publication Date:  March 01, 2021

The purpose of this study is:

Studying the Ser/Thr phosphorylation mechanism effects on mammalian target of Rapamycin FOX binding mechanism pathways for removing insulin resistance and recover tumor cancer cells and understanding that pyrimidine (Thymine, Cytosine) are playing imp rules in tumor cells cancers recoveries, and the Ser /Thr amino acids are the Phosphorylation regulators tools effects on pro-mTOR bind to FOX genes for producing the four kinds of protein kinases, for S6K1 genes synthesis, for ribosomal p70S6 kinase reactivations, and insulin productions.

Abstract
MTOR genes are originated and activated from ribosomal genes S6K1 and p70S6 with mitochondrial contributions. mTOR pathway is considered a necessary tool for regulating and activating necessary cellular pathways by which eukaryotic cells adjust their protein biosynthetic capacity for nutrients needs and availability.

The necessary phosphorylation processes on pro-mTOR protein lead to the production of four kinds of protein kinases for running and regulating most of cellular metabolism and for 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 kinds 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.   The increasing of  AMPK activities will be for the Akt synthesis priority by attracting and using phosphorylation processes for  Akt synthesis from PSTG protein kinase then for GTPase pathways productions.

Cardiac arrest is due to increasing in ATPase with severe reductions in G-protein kinase and GTPase productions and increasing in +ve molecules in genes inside cells that will lead to an increase in cells sizes that will lead to precipitation of protein molecules in blood vessels due to decreasing in blood vessels permeability area regards to its normal sizes, that will lead to sudden cardiac arrest depending on the number of precipitated molecules and on the decreasing in arteries cylindrical sizes, means that your heart can suddenly stop beating in case of G-protein kinase reduction and reductions in GTPase resynthesis.

This cuts off blood flow to the brain and other organs. It’s an emergency and is deadly if not treated immediately through re-increasing. GTPase and G-protein kinase with tyrosine kinase proteins, where GTPase with proper sequences are so necessary for Endosome and Golgi transport. Where GAPs coexist in most cells, that responsible for increasing the diversity of signals that regulate internal and external cellular pathways cycles.

The decrease in Akt molecules which are derived and synthesized mainly from G-protein kinase "PSTG" (and tyrosine kinases) with increasing in +ve molecules in the same protein can help the heart restart its activities.

Also, increasing +ve bonding energy & its positive molecular binding energy in any of the four kinds of protein kinase produced from pro-mTOR can lead to decreasing in their main active pathways and can be the main reason for heart disease problems.

Insulin resistance is due to decreasing or inhibition in the tyrosine kinase productions and pathways activities, and may associated with mitochondrial dysfunction too, which can show increasing in PSTA protein kinase productions and its pathways activities with reduction or inhibition in tyrosine "PSTT" protein kinase productions and pathways activities.

Materials

pro-Mammalian rapamycin bind with nutrients molecules (pro-mTOR)

_, G-protein kinase (PSTGk) , tyrosine kinase (PSTTk) , Cytosine kinases (PSTCk) , adenosine protein kinase (PSTAk)

_ mammalian Target of rapamycin complex subunit MLST8,

_hydrophobic amino acids, and Ser/Thr amino acids,

_Proto-oncogene, serine/threonine kinase PIM1

_mammalian target of rapamycin complex 1 and 2 (mTORC1, &mTORC2)protein kinases , Akt active proteins kinases , adenosine protein kinase, tyrosine (Thymine S/T kinases) active protein kinase,

_phosphatidylinositide 3-kinase (PI3K)

_inner cells chromosomal  13q14 gene,

_lysosomal security granules, and mitochondrial effective synthetase enzyme,

_inner ribosomal p70S6 genes

_eukaryotic initiation factor 4E binding protein 1 (4E-BP1),

_70-kDa ribosomal protein S6 kinase (S6K1) 

_FOX forkhead genes

_ROR alpha genes

_GTPase genes

_ATPase phosphorylation tool

_cholesterol productions regulated by FOX and ROR alpha genes

_ insulin regulated and produced by pro-mTOR _FOX binding mechanism pathways

_enkephalin  Leu-pentapeptides and Meth-pentapeptideactive genes

 
Introduction

The mammalian-target-of-rapamycin (mTOR) is multidomain protein kinases that are so important in regulating several cellular metabolic pathways including translational machinery.

mTOR complex 1 (mTORC1) and 2 (mTORC2), has a fundamental role in coordinating anabolic and catabolic processes in response to growth factors and nutrients (1).

Mammalian target of rapamycin (mTOR) protein pathways is activated by specific amino acids, by insulin,  and by growth factors.

When insulin digest its cholesterol substrate  (which regulated by ROR alpha genes and by FOX transcription factor genes), the mTOR protein will be reactivated again through ribosomal p70S6 +S6K1 genes translations activities with mitochondrial inner membrane functions with the contraction of  GTPase regulations functions for re-running regular mTOR biological cycles for normal insulin growth, for reactivating and repair the mitochondrial membrane, for pyrimidine resynthesis, for the rebuilding tyrosine leucine and other hydrophobic amino acids for estrogen and insulin synthesis, for rebuilding sestrin-Leu 1 genes through binding with FOX forkhead genes, and for re stabilizing FOX forkhead active genes with ROR-alpha genes.

mTOR acts as a ‘master switch’ of cellular anabolic processes and energy-producing catabolic activities including energy-intensive.

It promotes cells and hormone growth in response to extracellular mitogen, energy, nutrient and stress signals but depending on the availabilities of AMPK protein and phosphorylations tools and mechanism by ribosomes and other actin ATPase tools.

mTOR functions within two distinct complexes mTORC1  & mTORC2, where, mTORC1 is considered involved in the regulation of the translations initiating machinery influencing cell growth including proliferation, while mTORC2 participates in actin cytoskeleton rearrangements and cell survival under regulation by mTORC1. MTORC2 is a complex formed by translations from mTORC1 which are regulated by FOX genes box stabilities and activities and from ROR-alpha genes activities too.

MTORC2 can be considered as a stored emergency complex and feedback process for recover mTORC1, for reactivating autophagy, and for performing signals messages through the availabilities of lysosomal security granules which is necessary for activating autophagy. 

MTOR complexes also considered as a synthesized protein kinase started from phosphorylation effects on pro-mTOR which originally produced from ribosomal genes or specifically subunits that will carry specific arranged sequences (have specific signals functions for ribosomes activities in several tissues) from ribosomal and mainly from 1st DNA strand and then will be modified and activated by mitochondrial membrane functions, then will follow the necessary cellular metabolic pathways.

MLST8 is the Target of rapamycin complex subunit LST8, also known as  G protein beta that can activate mTOR by the reactivities of GTPase and AMPK protein pathways.

RHEB is also known as Ras homolog enriched in the brain (RHEB) is a GTP-binding protein that is ubiquitously expressed in humans depending on the availabilities of G-protein kinase, which normally is involved in the mTOR protein for the regulation and reactivate G-protein kinase synthesis for brain functions and for reactivating cellular metabolic depending cycles.

Activated FOXO-mediated insulin resistance is blocked by reduction of TOR activity, indicating pro-mTOR produces tyrosine kinase and G-protein kinase that should involve FOX forkhead stabilities and function for cholesterol synthesis for new insulin production and inhibit old insulin-like productions. (2).

mTORC1 inhibition, (in addition to reducing protein synthesis), deeply affects gene transcription and initiates autophagy 07, where indicates that the active mTORC1 can contribute to cell stress.

Through the binding mechanism of mTOR to FOX for purifying its composition for generating the four necessary active proteins kinases:  G-protein kinase (PSTGk), tyrosine kinase (PSTTk), adenosine protein kinase (PSTAk), and Cytosine protein kinases (PSTC K), those kinases will follow metabolic pathways for genes and alpha subunits productions, for ATPase and GTPase productions,  for antigen reactivations, and for cholesterol productions which will be the substrate for estrogen and insulin growth and productions.

Through the binding mechanism of mTOR to FOX for purifying its composition for generating the four active proteins kinases, the Sestrins-Leu 1 will be produced,  the adjusting of blood purines will be started by the mitochondrial synthetase and synthases enzymes by converting extra purines nucleotides to active pyrimidine nucleotides for reactivating the necessary hydrophobic amino acids and other necessary amino acids as Ser /Thr synthesis, and the limited ribosomal ATPase will be activated depending on the quality and quantity of the three kinases PSTGk, PSTT& PSTAk productions from the main pro-mTOR protein, then the GTPase will be activated for reactivating mitochondrial inner membrane and for its necessary pathways regulating activities.

The G-protein kinase pathways have the priority of using phosphorylation tools and kits instead of mTORC1 synthesis pathways where (PSTG) Kinase metabolic pathways have the priority in the metabolic process than other Cytosine kinases pathways, where can lead to delaying (but not inhibition) the Cytosine protein (PSTC) kinase pathways which needed for the mTORC1 production and the autophagy productions.

The increase in G-protein kinase activities will reflect the reductions in the tissue stress with increasing in sestrin-Leu 1 production, and increasing in adjusting the purines and branched fatty acids by mitochondria and contribution of some other genes and alpha subunits through the conversion of extra purines to pyrimidine nucleotides for building necessary amino acids for kinases protein synthesis and activities in the necessary cellular metabolic pathways and necessary genes signal activities through interstitium tissue fluid to several tissues.

The MTORC2 involved in cells proliferation and survival, cell migration and cytoskeletal remodeling which modulated by mTORC1 (with the modulation of PSTTk, and PSTGk ), which indicated that the presence and protection of mTORC2 are so imp for autophagy activities but with modulations of PSTCK, PSTTK, and PSTG kinases active protein.

The mTORC2 complex  consisting of seven protein subunits, that, rictor  Gene, is necessary for ribosome binding and has the activity of protein kinase binding and found only in mTORC2  (3,4). It has been considered that the scaffold protein is substrate binding to mTORC2, which indicates the necessity of mTORC2 for autophagy activities and regulations.

In another hand, mTORC1  considered being the modulator  and regulator subunits for mTORC2 complex, that if reduced or inhibited will lead to free mTORC2  from mTORC1 modulations or mainly will be free from ribosomal S6K1 and from p70S6 genes modulations and necessary activities, that autophagy can be activated under modulations  of other foreign genes (as toxic viral protease or other toxic factors ), that autophagy will be activated irregularly  without being regulated or modulating by original  inner cells as inner ribosomal necessary genes (as active p70S6 ribosomal genes) , and without regulation by serine/threonine-Cytosine

Kinases Proteins (PS/TCK  ) Proteins that modulate the mTORC1 synthesis will not be repaired again or will not be monitored. 

The inhibition of mTORC1  due to deficiency in pyrimidine active nucleotides or due to deficiency in hydrophobic amino acids will reflect the beginning and early decreasing in the specificity of autophagy to its living cells cellular cycles protection, and reflect the decreasing in autophagies belongisties and specificities to their original living cells, and can reflect early decreasing in sestrin-Leu 1 reactivities, with decreasing in FOX forkhead genes stabilities and inhibition in its imp regulations for cells proliferation survival,  and migrations, and cytoskeletal remodeling pathways.

The active mTORC1 kinase protein which depends on the presence of active cytosines nucleotides and active hydrophobic amino acids with the availabilities of the presence of Serine and threonine amino acids that has its necessary regulations processes for cellular metabolism activities, and originated from the  Pro-mTOR due to phosphorylations processes to produce the four kinases proteins in response to signaling pathways (where, signaling pathways can start by brain enkephalin pentapeptides activities, or with G-actin and its ATPase activities ), and will be de-regulated in many human diseases where there were sever decreasing in Pro-mTOR-FOX binding activities pathways for cellular activities, and there was a severe deficiency in one or more of protein kinases productions specifically in PSTT, PSTG and in PSTC kinases Proteins.

Pro-mTOR protein metabolic pathways can be reactivated by phosphorylation processes by using the mechanism of Phosphorylation of serine/threonine amino acids in the mTOR protein chain for the productions of the necessary four kinds of protein kinases.  

The serine/threonine-protein kinase PIM-2 (one of three PIM kinases) indicated its necessary functions for autophagy activities that are involved in its regulations, which was initially discovered as a regulator of glycogen synthesis and has also been found to be involved in autophagy modulations (5).

Where, PIM serine/threonine kinases can be considered as active subunits sequences involved in the four kinds of protein kinases specifically in PSTC, PSTT, and PSTG Kinases Proteins for increasing their activities due to phosphorylation processes during the binding with FOX genes and play an important role in healthy cellular metabolic pathways as in anti-inflammatory processes, and in ribosomal genes resynthesis. That protein ser/Thr (PST) kinases can increase the modification of increasing of specific substrates including several cellular regulators and apoptosis mediators.

PIM1 but not PIM2  can increase the migration of normal and malignant hematopoietic cells by regulating chemokine receptor surface expression where PIM1 is the main regulator but PIM2 is the tool for PIM1 regulations as mTORC2 is the tool for mTORC1 regulations activities.

Proto-oncogene, serine/threonine kinase PIM1 is the products from Phosphorylation used the ser/Thr mechanism during the binding of pro-mTOR mTOR with FOX forkhead genes, where PIM genes is holding and monopolies the main amino acids and arranged sequence for running the phosphorylation mechanisms for producing the four kinds of protein kinases.

The PIM is the key to contributing to the formation of four proteins kinases, that each of sre/Thr (Ser:TCT, TCC, TCA, TCG /Thr: ACT, ACC, ACA, ACG) contain its specific triplets, where only Ser contains the Thymine nucleotides but not threonine, where deficiency in Ser will reflect a deficiency in Thymine nucleotides metabolic pathways, and thus will force cellular cycles to use threonine phosphorylation mechanism in case of its availabilities in cellular metabolic pathways.

Each of those produced active protein kinases will begin with a specific nucleotide at the beginning of its protein sequences chain that will characterize its functions and specificities in cellular pathways activities and will characterize the main variations between those protein kinases within pathways functions.

The main involvement of those two amino acids of Ser and Thr in most of the phosphorylation mechanisms of proteins regulations  is the containing of Cytosine in the middle of their triplets that will facilitate the binding of cytosine to phosphorus then release  adenosine, Thymine, and guanine upon phosphorylation effects on pro-mTOR proteins, where at the Phosphorylation effects will act on Cytosine bind to phosphorus to release the other  nucleotides for the production of the four kinds of protein kinase:

1) G-protein kinase (PSTG Kinase) 

2) adenosine kinase PSTA Kinase which will activate ATPase cycles that will begin with adenosine nucleotides, 

3) Tyrosine kinases (PSTT Kinase ) which will activate Leu (TTG Or TTC) and  other hydrophobic amino acids including tyrosine with some other necessary amino acids (depends on the presence of Thymine nucleotide in their triplets eg: PRO (TCC), Cys (TGT), Tyr (TAC or TAT), Arg (CGT), Ser (TCT or TCC or TCA), Gly (TGG), Asp (TAG), Ala (TCG), Val, (TTG), Ser (TGA), Asn (TAA), Tyr (TCA), Île (TTA), His (TAC),

4) The Cytosine kinases (PSTC Kinase )  that can produce  mTORC1 which can activate tRNAs and autophagy that their activities depend on the presence of cytosine nucleotides in the composition of their genes which necessary for migration functions.

Notice, may one or more of those protein kinases can be produced more than others depending on the quantity and quality of nutritions molecules and depending on the produced enzymes and active genes by chromosome and regulated by the ribosome, by mitochondria, and by the stabilities of both ROR alpha genes and FOX genes, that may have more  threonine (ACA or ACG) than Ser (containing Thymine), that will produce more adenosine kinase with a deficiency in tyrosine kinase and in cytosine kinases that will reflect a problem in cellular metabolic pathways as breast cancer and maybe the main for capillaries blockage and Narrowing of the aorta, atherosclerosis, and failure in functioning branched fatty acids.

The production of tyrosine-protein kinase PSTTk due to phosphorylation on pro-mTOR protein will be derived for regulating specific cellular activities, where PSTT is necessary for leucine synthesis re-activities in several cellular pathways and for reactivating enkephalin Leu pentapeptides activity in the brain, and can be the regulating tools for antigen re-synthesis, and will be necessary with Leucine amino acids for regulating sestrin-Leu 1 synthesis during FOX genes binding regulation.  Some of the produced nucleotides from amino acids due to Phosphorylation can be so necessary for protein synthesis, for enzyme productions, and for gene synthesis.

The G-protein kinase (PSTG) can activate  ribosome and  mitochondrial inner membrane through GTPase regulations, also G-protein kinase will be the stimulator for insulin secretion and productions, that the mitochondrial GTP (mtGTP)  synthesized by succinyl-CoA synthetase (SCS) is hydrolyzed via mitochondrial PEPCK (PEPCK-M) to make phosphoenolpyruvate, a high-energy metabolite that integrates TCA cycling and anaplerosis with glucose-stimulated insulin secretion (6)

The role of PSTGk, PSTTk, and PSTCK in modulating mTORC1 production is for modulating and regulating tRNA too, and for regulating mTORC2 productions for tRNAs and for autophagy synthesis and reactivities, where phosphatidylinositide 3-kinase (PI3K) and mTOR complex 2 (mTORC2) are acutely activated by aa-readdition in a mTORC1-independent manner (7).

The mammalian target of rapamycin mTOR, plays a critical role in maintaining a balance between cellular anabolism and catabolism throughout phosphorylation mechanism processes, through the binding mechanism to FOX forkhead genes, and through the effect of mitochondrial enzymes productions on pro-mTOR protein.

Where, the FOX-mTOR binding processes is necessary for the kinases protein productions, for sestrin-Leu 1 productions due to phosphorylations Ser/Thr mechanisms, for  AMPK production, and then for  mTORC1 production which regulate mTORC2 productions for autophagy and for tRNAs reactivation.

 FOX gene subgroups transcriptional disturbances affecting numerous complex molecular cascades, and have been linked to a wide range of cancer, that indicate the importance of re-stabilities of FOX forkhead genes by the phosphorylations binding mechanism to pro-mTOR with the regulations of ribosomes and mitochondria for producing the four kinds of protein kinases which are so necessary for modulating and running cellular metabolic pathways.

The pathogenesis of colorectal cancer (CRC) is especially due to a deficiency in necessary nucleotides responsible for G-protein and for PSTA protein kinases production, where deficiency in Thymine, Cytosine nucleotides and in hydrophobic amino acids with a deficiency in Ser amino acids will show genomic instability, chromosomal aberrations, and DNA promoter hypermethylation. CIN tumors (  are found on the surface of the cervix, and are usually caused by certain types of human papillomavirus {HPV} ) show chromosomal gains and losses and structural rearrangement (8).

CIN tumors indicate the origin of irregularities in Ribosomal ATPase molecular composition due to deficiency in Ser amino acids in the Ser/Thr phosphorylation mechanism, then consequently will reflect a deficiency in one or more of protein kinases productions, where are necessary for reactivating ribosomes and mitochondria inner membrane. The CIN reflect a specific mutation in the

rRNAs due to the deficiency in Thymine and or Cytosine nucleotides (depending on the cases and types of the missed amino acids ) that reflect a deficiency in FOX genes stabilities and functions, and deficiency in protein kinases production which are necessary for ribosome mitochondrial inner membrane repair and stimulations, and are necessary for FOX forkhead genes stabilities and functions for regulating sestrin-Leu 1 synthesis, for cholesterol productions, for S6K1 productions, and for reactivating AMPK protein.

Colorectal cancer can start with a blockage in capillaries leads to isolation to specific intestinal cells with a deficiency in one or more hydrophobic amino acids and in protein kinases produced by phosphorylation on pro-mTOR, which can lead to inflammation in goblet cells. Decreasing in the PSTG with PSTA Kinases protein can lead to a reduction in ATPase production and in GTPase activities that lead to mutations in rRNAs which can be spread.

The deficiency in mTORC1 regulation activities will reflect a reduction in the migration of protein molecules lead to tumor. The reduction in GTPase activities will lead to increasing in cell size and decreasing in ribosome activities where GTPase are needed for modulating most of the cellular metabolic pathways, that the PSTG Kinase pathways have the priority for using the Ser/Thr phosphorylation mechanism for Akt production and for modulating the GTPase activities. mTOR signaling is activated indirectly by hormones and growth stimulated factors, where signals are negative charges started by ribosomes and by G-actin negative  ATPase small subunits to be sent through inner cells to start mTOR synthesis that will carry all cells needs throughout its created protein sequences that will be derived to the bloodstream to reconnect and united with nutrition absorbed molecules and rebind with FOX forkhead genes for reforming the for kind of protein kinases.

cholesterol synthesis is regulated by FOX and ROR alpha genes through the production of PSTA, PSTG, PSTC, and PSTT kinases protein during phosphorylation Ser/Thr mechanism on mTOR, and the AMPK is activated during the same metabolic cycles for running the full active cellular pathways, where at time of  decreasing in insulin the cholesterol which is its substance will be synthesis  to reactivate insulin growth, where mTOR can be stimulated and affected by the PI3-kinase pathway and PKB/Akt (9).

During FOX-mTOR binding the pyrimidine synthesis from purines will activate by synthetase mitochondrial enzyme to contribute to the presence and availability of needed pyrimidine nucleotides for genes and protein synthesis including S6K1 genes and GTPase productions, where the tumor growth and contents can reflect the reductions in G-protein kinase and in PSTG Kinase pathways then consequently will reflect reductions in GTPase which will lead to increase in cells size and in its protein contents.

The Forkhead box O (FoxO) transcription factors are downstream targets of the serine/threonine-protein kinase B (PKB)/Akt, which regulates processes of cellular proliferation and survival (10). And FOX genes are regulator genes for the four kinds of active protein kinases for running the protein and genes synthesis including the autophagy and tRNAs activation. The fact that the mTORC1 deregulation and reductions in autophagy are associated with several human diseases, such as type 2 diabetes, cancer, obesity, and neurodegenerative (11).

FOXO3a activity is regulated by the activation of (nucleus and mitochondrial activities, where through the binding of mTOR to FOXO1 will produce mTORC1 complex and other "PIMs" proteins kinases. The stimulations and activations of FOX genes by chromosome and by mitochondria indicated that FOX genes have arranged gene sequences qualified for regulating all protein kinases productions and activities pathways including S6K1 and estrogen hormone synthesis pathways. The activated  FOXO3a can induce autophagy effectors, gluconeogenic enzymes, and others (12) because mTORC1 which produced from the regulated PSTC kinase protein is having the same arranged regulated sequences from FOX genes and from the nucleus which is main for regulating autophagy activities and synthesis, sp any Disturbance or turbulence to those sequences will case effects in their produced products genes.

On the other hand, upon glucose restriction, 5′-AMP-activated protein kinase (AMPK) and mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) -dependent FOXO3 and mitochondrial translocation allows the transcription of oxidative phosphorylation (OXPHOS) genes, restoring cellular ATP levels (12)

Sestrin1, AMPK Autophagy, and more of activated proteins and genes by FOX genes which result from mTOR-FOX forkhead genes binding under modulations and regulations by phosphorylation Ser /Thr mechanism (PS/TM), mitochondrial enzymes effects, and ribosomes ATPase activities, are all mainly regulated by a nucleus, and regulated by ribosomal functions and activities depending on PS/TM, where the synthesized genes as S6K1  gene will derive to the inner chromosomes and ribosomal inner genes to ensure its genetic original compatibility with the ribosome and with chromosome and to restore the original compatibility if differences occurred in it as a result of inner cell metabolic processes.

The genes for the paired box proteins PAX3 and PAX7, respectively, can be fused to the FKHR (forkhead in rhabdomyosarcoma) gene on chromosome 13q14 (13), where the chromosome 13q14 deletion syndrome is characterized by the retinoblastoma, variable degrees of mental impairment, and characteristic facial features, including high forehead, prominent philtrum, and anteverted earlobes, and indicate that the chromosome 13q14 gene is the main for ribosomal activities, for ROR alpha genes, and for FOX genes regulations and their produced genes and active proteins products and activities.

Figure 1

Figure 2

Figure 3

Methods:

The translational repressor, eukaryotic initiation factor 4E binding protein 1 (4E-BP1), and the 70-kDa ribosomal protein S6 kinase (S6K1)  are important tools of protein and hormone synthesis pathways, and together they have and play regulations behavior of both eukaryotic initiation factors and ribosomal repairs and activities.

Please refer to the attached pdf to view the complete article

 Volume 2 Issue 3 March 2021

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