Rac1 AT1 Required For Ang2-AT2 Activities For Cardiomyocytes And ECs Where Tyr TAT And TAC Kinases Required For Preventing Glycoprotein Storage And Glycogen Accumulation

Active Rac1 are so imp for improving cytoskeletal systems and for improving anti-inflammatory processes by activating Plcγ2, IFN-beta and glucocorticoid-beta (which necessary for B arrestin synthesis which necessary for activating endothelial cells function through activating ACE functions). Tyrosine kinases function (contain TAT and TAC codons) are so necessary for activating Ang2-AT2 productions for adjusting heart contractions and preventing collagen, glycoproteins, and cholesterol accumulations. Angiotensin II type 2 receptors (Ang2 bind to AT2 receptors) are produced from Ang1-AT1 by ACE regulated functions in Tyr kinases-dependent Abstract BTK and Ang1 AT1 are so necessary for IgM and IgG3 synthesis in blood serum that can be considered as so necessary for anti-inflammatory improvement, but in case of the absence of Tyr Codons TAT & TAC (kinases) the BTK will be critical for increasing the accumulated collagen (accumulated glycoprotein) in arteries which are critical for the tumor synthesis. Glycogen storage disease (GSD) and glycoprotein storage disease (GSD) are started by sever deficiency in Tyrosine TAT and TAC pyrimidine kinases (which reflect deficiency in Ang2-AT2 productions) that will lead to accumulated glycogen (increasing in Ang1 AT1 activity and glycoprotein accumulations), where, Ang2-AT2 productions are necessary for binding to the stored glycogen with metalloproteinase dependent for platelets activation mediated by releasing nitric oxide. 5-hmC are considered as the enhancers and the key regulators in heart developments, contractions, and blood vessels protections, where 5-hmC regulated by pyrimidine kinases and is so necessary for adjusting muscles contractions through methylation and demethylation processes. cause will (pyrimidine kinases) which play important roles in building dynamic promoters in Ang2-AT2 active molecules. The deficiency in pyrimidine synthesis due to deficiency in synthetase functions will cause deficiency in pyrimidine kinases and mutations in thymine kinases and in cytosine pyrimidine kinases. Also deficiency in pyrimidine kinases will lead to increasing in Ang1-AT1 activities ” that will promote maturation including allergic inflammations and tumors mediated by mutated CTGF productions and will associated with decreasing in signals productions (necessary for adjusting heart beats. Also deficiency in Estrogen productions (due to decreasing in pyrimidine kinases with increasing in purines kinases) that will lead to cholesterol accumulation and decreasing in B-arrestin that will not activate ACE for reactivate endothelial cells function. then dropping in blood pressure. Note that increasing in adverse ventricular (LV) dilatation due to inhibition or deficiency in Ang2-AT2 synthesis (deficiency in pyrimidine kinases) will lead to increasing in Myocardial relaxation time that will be main reason in hypotension which due to increasing in ventricular volume leads to an increase in the diastole of the heart due to increasing maturation and proliferation by Ang1 AT1 that lead to Vascular blockage and vasocon striction and arrhythmogenecity that (depend on the percentage and type of Ang2-AT2 inhibition. Inhibition in pyrimidine kinases will lead to inhibition in Ang2-AT2 that can lead to increasing in glycoprotein storage in blood vessels (and glycogen accumulation) and can lead to increasing in left vertical size and sudden cardiac arrest. The mutated Angiotensin II which lack Tyrosine TAT and TAC codons has the activity of enhancing endothelin-1-induced vasoconstriction through decreasing its control to Ang1 AT1 proliferative activities and will lead to glycoprotein and glycogen accumulation in blood vessels with decreasing in platelets activation (which regulated by Ang2 AT2 binding to glycogen in metalloproteinase dependent). The inhibition in Ang2-AT2 functions means Endothelin A (ETA) receptor blockade that will lead to glycoprotein storage and glycogen accumulation in Blood vessels (depend on the quantity and type of Ang2-AT2 inhibition) that can promotes adverse ventricular (LV) dilatation (depends on the percentage and the type of tissues that contain the Endothelin A (ETA) receptor blockade). But, abnormal Angiotensin II which Deprived of the availability of necessary Tyrosine Codons TAT and TAC kinases will enhances endothelin-1-induced vasoconstriction through enhancing the Ang1-AT1 activities that will lead to glycoprotein perception in blood vessels and increase CMs activities with failing or decreasing in ECs functions. due (CMs) endothelial PLCγ2, AT1 Ang2-AT2 by Tyr kinases functions and Gp GTP subunits synthesis (Rho family) promote ECs adjust and hyperglycemia and preventing glycogen followed cells and The necessary Tyr Codons TAT codons followed by TAC codons are necessary for building promoters in Ang2-AT2 (which considered as C-protein responsible for migrating molecules and adjusting signals for adjusting Myocardial contraction and relaxation) ، where the increase in protein C which contain Tyr TAC Codons can disturb the interstitium fluid processes due to stimulation the methylatiions and demethylations process which affect heart contractions. It is approved that the Angiopoietin-1 a Ligand for the TIE2 Receptor is required during Embryonic Angiogenesis Where, Tyr kinases (contains necessary Tyr Codons) are necessary for activating Angiopoietin-1 for modifying its own crucial roles throughout building the TAT and TAC in the Ang2-AT2 (Ang2-Tie2) molecules productions (regulated by ACE domains functions) in mediating reciprocal interactions between the endothelium and surrounding matrix. Ang2 is necessary to bind with Tie 2 to form Ang2-AT2 receptors expression (regulated by Tyr kinases) which are so necessary for adjusting heart contractions and efficiency that has the unique functions for preventing the deposition of glycoprotein and glycogen in blood vessels.and tissues. That, Angiopoietin-1 (Ang1) binds to and activates endothelium-specific receptor tyrosine kinase "Tie2", that Ang1-Tie2 signal has been proposed to exhibit two opposite roles in the controlling blood vessels That the of Ang2-AT2 is upon the effect of Converting Enzyme ACE will activate two opposite Pathways: previous study the importance of Ara-cytosine in activating glutamine synthetase, where the inhibition in cytosine will result of glutamic accumulation that reflect failure in heart function and neuronal toxicity.But availability of cytosine 5 will adjust the in purines and accumulated glycoprotein by acting on purines for producing nitric oxide which activate G-actin and release signals which adjust heart contraction and