Inhibition Plcγ2 and Hydrophobic Acids Synthesis cause Osteoarthritis, Diabetes and C-lymphocytic Leukemia Diseases Where Normally PLCs can Recover Interferons Synthesis

Abstract

Proper S6K regulate BTK pathways which regulate PLCγ2 synthesis which are main regulations for thromboxane-A “TXA2” synthesis, and necessary for B-cell maturations and T-cells modulations and functions. Deficiency in Ser amino acids and in hydrophobic amino acids are reflect decreasing in synthase enzyme lead to deficiency in BTK function and deficiency in PLCγ2 that lead increasing in colony stimulating Factor-1 “CSF-1 where PLCγ1 specified to circuit to CSF-1 which upon synthase effect will promote PLCγ2 synthesis which necessary for activating BCRs for activating both IgM and IgD antigen for B-cells maturation and activities, for T-cells modulations, and for TXA2 synthesis. Proper Akt, S6K1 synthesis, OPA1 enzymes and fatty Acyl-COAs are necessary for regulating RORs isoforms Biosynthesis which regulate both IFNs and PLCs synthesis {Where both IFNs and PLCs are covering each other (IFNs <¬>PLCs) } that PLCγ1 promote the PLCγ2 synthesis upon BTK regulations. Osteoarthritis “OA” is characterized by a sharp expression in Gamma-Phospholipase C-1 “PLCγ1”, with decreasing “or inhibition” in PLCγ2 which reflect decreasing in synthase functions and in IFN-beta synthesis that reflect decreasing or deficiency in TXA2 Biosynthesis. The increasing in PLCγ1 with Deficiency in Ser amino acids will lead to deficiency in Ser phosphorylation signaling and deficiency in the pyrimidine kinases (PST-thymine and PS T-Cytosine kinases) synthesis, that lead to decreasing in synthase activity which will reflect down regulations in BTK pathways and inhibition in PLCγ2 productions which will reflect diabetes ( production of Androgen instead of estrogen), and can reflect Osteoarthritis “OA” prognosis which depend on the percentage of Deficiency or inhibition in basic amino acids and their basic necessary signaling pathways. T2DM is strongly connected with OA diseases and are linked together by the deficiency in Ser amino acids and their phosphorylation, and any early decreasing in Ser and in hydroponic acids synthesis can lead to both and more disease. Pathogenic type 2 diabetes associated with progressive beta-cell impairment due to the mutations in the production of S6K1 (deficiency in Ser ”TCT, TCC,TCA”), and inhibition in the PLCγ2 which due to inhibition or decreasing in Synthase and lead to deficiency in BCR activities. The decreasing in PS/T-Thymine Kinases and PS/T-Cytosine kinases chains (mTORC1) due to deficiency in Ser amino acids (where normally those pyrimidine kinases are produced from the phosphorylation process on Ser amino acids) will lead to mutated S6K and Akt productions and decreasing or mutations in ATPase and GTPase which lead to decreasing in OPA1 repair and lead to synthesis of Androgen instead of Estrogen which are depending on the availability of hydrophobic amino acids synthesis including Ser and Tyr amino acids. The effect of Synthetase enzymes on biological molecules is for creating active gamma-subunits “PLCγ1” that can be modified by synthase effect for Betasubunit synthesis “PLCγ2” then will be modified by phospholipase effects for alpha subunits productions. The releasing of pyrimidine kinases “PS/T-Thymine -Kinase and PS/T-Cytosine -kinase chains (mTORC1)” are so necessary steps for proper S6K productions and for proper fatty Acyl-COAs synthesis (long fatty AcylCOA) which are so important for regulating RORs Biosynthesis and necessary for both IFNs and for PLCs productions which started by the productions of PLC-gamma and IFN gamma, where both PLCγ1 and IFN-Gamma are necessary for regulating proper PLCγ2 biosynthesis upon “BTK activity” then PLCγ2 are necessary for regulating BCR functions which imp for regulating both IgM and IgD activities for B-cell maturations, for adjusting anti-inflammatory processes and for T-cells modulations, then PLCγ2 is so necessary for thromboxane-A synthesis, and for bone growth and immune modulations. Deficiency in conversion of glutarate to glutamate and decreasing in Proline (hydroponic acids) biosynthesis can affect on Cartilage synthesis and bone growth due to decreasing in stimulating mitochondrial OPA1 oxidations. Protein tyrosine phosphatase (PTP) gamma (carry−ve charge regulated firstly by synthetase gamma-oxidations) has been proposed to be an important regulator for chondrogenic patterning, where PTPs are critical regulators of tyrosine phosphorylation that it’s activity depends on the Tyr, and Ser synthesis (during hydrophobic acids synthesis ) and on JAK state signaling activities. And so, the proline-rich tyrosine kinases regulate proper PLCs isoforms which compete for binding site at the very C terminus of fibroblast growth factor for osteorogenitor embryonic development, and bone growth.