Rac1 Rich Proline are OPA1 Flux Influencer for PLCs and IFNs Synthesis where Immune and Toxicity Due Deficiency in Synthetase and in Proline Synthesis

Tantawi, Ashraf Marzouk El

doi:10.47363/jjcmr/2022(2)132

Cited by 4 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rac1 are so necessary for regulating IFN-beta and PLCγ2 which necessary for TXA2 synthesis and platelet activation where, fibrin imp for activating CMs and endothelial cells: That PLCγ2 has necessary functions for regulating TXA2 and reactivating platelets [10].…”

Section: Introduction and Methodsmentioning

confidence: 99%

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

Tantawi¹

2022

J Cardiol Res Rev Rep

Self Cite

View full text Add to dashboard Cite

Active Rac1 are so imp for improving cytoskeletal systems and necessary for activating IFN-beta & Plcγ2 (which are necessary for regulating TXA2 Synthesis), and are playing imp role for activating CMs and endothelial cells through Ang1 synthesis (mediated by Gp GTP subunits synthesis) then followed by tyrosine kinases function (contain TAT and TAC codons) for Ang2-AT2 productions for adjusting heart contractions and preventing collagen, glycoproteins, and cholesterol accumulations. Angiotensin II type 2 receptors (AT2 receptors) play a modulatory role in blood pressure regulation but produced from Ang1-AT1 by ACE regulated functions , where Tyr codons are playing imp roles in AT1 and AT2 activities and can play so important roles in protecting heart and blood vessels from accumulated cholesterol and glycopeptides and from accumulated glycogen. AT1 receptors promotes the adjustment of various intracellular signaling pathways through Ang2-AT2 production resulting in hypertension, endothelial dysfunction, and recovering the cellular damage.

show abstract

Section: Introduction and Methodsmentioning

confidence: 99%

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

Tantawi¹

2022

J Cardiol Res Rev Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…And, previous studies indicate that 5-HT stimulated angiogenesis through activation of Akt in ECs [90]. And, Serotonin/5-HT1A Signaling in the Neurovascular Unit Regulates Endothelial CLDN5 Expression and, serotonin 5-HT regulates the balance of Th17/Tregs and promotes M2-polarization of macrophages and has a direct or indirect regulatory effect on traditional immunocytes such as T cells, macrophages, DC cells, and NK cells [91,92].…”

Section: The Role Of Serotonin In Activating T-cells and Promotingmentioning

confidence: 97%

DCs- IL2 Necessary for Glucocorticoids Which Necessary for Interferons Synthesis and Serotonin Synthesis then Promote Ang2- At2 and VEGF-A for Anti-Inflammatory Growth

Tantawi¹

2022

Jap J Clin & Med Res

View full text Add to dashboard Cite

Dendritic cells (DCs) play an important role in improving and adapting immune responses, and development of chronic inflammation through producing Interleukin-2 which stimulate beta oxidation processes by OPA1 synthase for promoting both IFN-beta and GC-beta production followed by alpha oxidations for TLR4 and SIRPα1 production and for nucleocytosolic acetyl-CoA alpha production which considered as signature of a “growth specifically for anti-inflammatory growth. Glucocorticoids and glutamine are the basic tools for increasing immune efficiency (regulated by OPA1 enzymes) and the main for regulating the adopted Interferons, that the deficiency in glucocorticoids synthesis and glutamine will suppress immune activities and will lead to deficiency in Interferons productions followed by decreasing in macrophages and T-cells functions. The formation of Glucocorticoid-gamma and IFN-gamma started by the effects of Cox2 on inflammatory sources followed by cytokine kinases production for IL2 synthesis upon synthetase functions followed by synthase for glucocorticoid-beta and IFN-beta productions which followed by phospholipase effect for producing PD-L1 synthesis which promote the progression of ovarian cancer.

show abstract

“…Where, studies reported that: Deficiency in pyrimidine kinases cause cholesterol accumulation and increase the risk of coronary artery disease [45].…”

Section: Figurementioning

confidence: 99%

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

M El Tantawi

2024

J Cardiol Res Rev Rep

View full text Add to dashboard Cite

Phenylalanine function stabilized by lysine which found on lysosomal surface, that Phe necessary to regulate the synthesis or secretion of α-amylase, trypsin and lipase, where the Severe acute pancreatitis in a child with phenylketonuria. The phenylketonuria due to decreased lysine followed by lysosomal dysfunction that will be result of deficiency in phenylalanine function that will not form pancreatic enzymes and stomach enzyme and will be accumulated. The Lysosomal dysfunction will be result of accumulation of undigested polymer including inflammation which play important roles in pathophysiology, that reflect reduction in lysine acylation followed by reduction in aminoacyl tRNAs which promote Phe and E coli functions for activating protein and mRNAs synthesis, that will be followed by increasing in TNf-a synthesis (and reduction in VEGF-As ) which activate NK (not beings related to human immune proper function ) which regulated by the undigested polymers in random pathways stimulated by TNf-a functional pathway (activated by NLRP3 inflammasome. Retinoic acid is necessary to promote lysine acylation which regulate aminoacyl-tRNAs production regulated by mitochondrial enzymes, which regulate mRNA production by E coli (regulated by phenylalanine) that necessary to run antioxidant functions and cellular biosynthesis. Lysine acetylation so important to regulates the activity of Escherichia coli Sadenosylmethionine synthase. RNA (produced by E coli) is 2′-O-methylated demonstrated higher stability that can improve immune by promoting anti-inflammatory processes and improve myocardial functions, and adopt heart constriction by activating NR4As pathway. The antihypertensive pathway mechanism is: the Lysine ¬¬>activate ATPase (stimulate retinoic acid “RA” ) ¬¬>Lysine acetylation ¬¬> promote Phe/ hydroxylase ¬¬> followed by ¬>activate Tyr/ hydroxylase ¬>activate dopamine ¬> activate NR4As pathway ¬>GC-beta ¬>activate both of Oxytocin and Nrf2 ¬> Ang2-AT2 and VEGF-A productive functions ¬>heme oxygenase ¬>anti-inflammatory growth and processes. Lysine Methylation has important role in adopt hypertension through activating pervious Antihypertensive pathway mediated by Phe hydroxylase synthesis and Tyr hydroxylase production followed by activating both of dopamine and NR4As pathway. The oxidation of phenylalanyl-tRNA synthetase positively regulates translational quality control, and regulates the initiation of digestive enzyme mRNA translation, where consecutive AAA-lysines is paused for encoding Phe followed by ribosome sliding on homopolymeric A sequence. That lysine activates mitochondria function followed by promoting Phenylalanine and phenylalanine-tRNAs productions by translations within E coli, followed by Phe/ hydroxylase activate Tyr hydroxylase production which activate dopamine synthesis. And positively, Lysine is the most effective amino acid for activating all of ATPase, GTPase, and lysosomes, and E coli functions, where ATPase necessary for activating lysine Phosphorylation for activating lysosome digestion, followed by activating E coli through activating Phe hydroxylase production, while GTPase necessary for activating mitochondrial repairs, which act on pro-inflammation and cholesterol for activating estrogen production and activating the NR4As pathway which activate all of Oxytocin, Nrf2 followed by Ang2-AT2 and VEGF-A production and then followed by activating heme oxygenase and anti-inflammatory growth and processes that prevent LV-hypertrophy, and prevent coronary calcification.

show abstract

Rac1 Rich Proline are OPA1 Flux Influencer for PLCs and IFNs Synthesis where Immune and Toxicity Due Deficiency in Synthetase and in Proline Synthesis

Cited by 4 publications

References 0 publications

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

DCs- IL2 Necessary for Glucocorticoids Which Necessary for Interferons Synthesis and Serotonin Synthesis then Promote Ang2- At2 and VEGF-A for Anti-Inflammatory Growth

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

Contact Info

Product

Resources

About