Inhibition in Proper Ser and In Plcγ2 Synthesis Are the Main for Causing Osteoarthritis, Diabetes, and C-Lymphocytic Leukemia Diseases

Ashraf Marzouk El Tantawi
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Abstract

Proper S6K /BTK and PLCγ2 synthesis (which regulated by Ser phosphorylation pathway) are main regulations for thromboxane-A “TXA2” synthesis, and necessary for B-cell maturations and T-cells modulations and functions. The main reasons for causing Osteoarthritis “OA” and diabetes diseases (that are linked together) are the deficiency of Ser amino acids and decreasing of Ser phosphorylation signalling pathway which necessary for proper S6K productions, where normally the Ser phosphorylation signalling pathway is the basis of Ser /Thr phosphorylation signalling and is necessary for proper Akt, S6K1 synthesis and necessary for RORs and IFNs synthesis and also necessary for running proper BTK for PLCγ2 productions , where S6K is main regulator for ATPase and for proper PLCγ1 and for PLCγ2 synthesis which necessary for bone growth and for modulating immune efficiency. Osteoarthritis “OA” is characterized by a sharp expression in Gamma-Phospholipase C-1 “PLCγ1”, with decreasing “or inhibition” in PLCγ2 “PLC beta” productions due to inhibition or mutation in S6K and then in BTK. The increasing in PLCγ1 with Deficiency in Ser amino acids will lead to deficiency in Ser phosphorylation signalling, and decreasing in synthase activity that will reflect down regulations in BTK pathways and lead to inhibition in PLCγ2 productions which will reflect diabetes (inhibition in Estrogen with the production of Androgen instead of estrogen) and can reflect Osteoarthritis “OA” prognosis depend on the percentage of Deficiency or inhibition in basic amino acids and its basic necessary signaling pathways.
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抑制适当的Ser和plc - γ2合成是引起骨关节炎、糖尿病和c淋巴细胞白血病的主要原因
适当的S6K /BTK和PLCγ2合成(受丝氨酸磷酸化途径调节)是血栓素- a“TXA2”合成的主要调控因子,也是b细胞成熟和t细胞调节和功能所必需的。导致骨关节炎“OA”和糖尿病疾病(两者相关联)的主要原因是丝氨酸氨基酸的缺乏和丝氨酸磷酸化信号通路的减少,而丝氨酸磷酸化信号通路是正常的S6K产生所必需的,其中丝氨酸磷酸化信号通路通常是丝氨酸/苏氨酸磷酸化信号通路的基础,也是正常的Akt所必需的。S6K1的合成是RORs和ifn合成所必需的,也是运行适当的BTK以产生plc - γ2所必需的,其中S6K是atp酶和适当的plc - γ1和plc - γ2合成的主要调节剂,这是骨骼生长和调节免疫效率所必需的。骨关节炎的特点是γ -磷脂酶C-1“PLC - γ -1”的急剧表达,由于S6K和BTK的抑制或突变,PLC - γ - 2“PLC - β”的产生减少或抑制。缺乏丝氨酸的plc γ - 1增加会导致丝氨酸磷酸化信号通路的缺失。合酶活性降低,反映BTK通路下调,导致PLCγ2产生抑制,反映糖尿病(抑制雌激素,产生雄激素而不是雌激素),反映骨关节炎的预后,这取决于基本氨基酸及其基本必要信号通路的缺乏或抑制的百分比。
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