Interaction Enhanced(交互增强)研究综述
Interaction Enhanced 交互增强 - The complex realities found were focused on comprehensive forms and contextualized in wheels of conversations with the protagonists of the research from the movements and moments of interaction enhanced by the Pedagogy of Alternation. [1] More importantly, mutations (R867Q, R867A and R867G) disrupted this interaction enhanced the activity of JAK2-STAT5 pathway and the proliferation of Ba/F3 and MV4-11 cells. [2] Additionally, we investigated the molecular mechanisms and demonstrated that RPS24c mRNA interacted with lncRNA MVIH, the binding-interaction enhanced the stability of each other, thereby activated angiogenesis by inhibiting the secretion of PGK1. [3]所发现的复杂现实集中在综合形式上,并在与研究主角的对话轮次中被情境化,这些对话来自交替教育学增强的互动动作和时刻。 [1] 更重要的是,突变(R867Q、R867A 和 R867G)破坏了这种相互作用,增强了 JAK2-STAT5 通路的活性和 Ba/F3 和 MV4-11 细胞的增殖。 [2] 此外,我们研究了分子机制并证明RPS24c mRNA与lncRNA MVIH相互作用,结合相互作用增强了彼此的稳定性,从而通过抑制PGK1的分泌来激活血管生成。 [3]
Synergistic Interaction Enhanced
This synergistic interaction enhanced the energy transfer and facilitated more excited excitons generated by SeAuFe-EpC NPs, thus promoting the transformation of 3O2 to 1O2via resonance energy transfer, finally resulting in irreversible cancer cell apoptosis. [1] This synergistic interaction enhanced the rigidity of the material (tensile stress ∼13 MPa) while maintaining high tensile toughness (∼58 MJ m−3). [2]这种协同作用增强了能量转移,促进了SeAuFe-EpC NPs产生更多的激发激子,从而通过共振能量转移促进3O2向1O2的转化,最终导致不可逆的癌细胞凋亡。 [1] 这种协同作用增强了材料的刚度(拉伸应力~13 MPa),同时保持了高拉伸韧性(~58 MJ m-3)。 [2]
interaction enhanced jak2
More importantly, JAK2 K607N and mutations disrupted this interaction enhanced JAK2-STAT5 pathway activation and the proliferation of Ba/F3 cells. [1] Mutations (T875N, T875A, D873A and D873G) disrupted the T875 and D873 interaction enhanced JAK2's activity, decreased its structural stability and JH2 domain's activity which further enhanced JAK2's activity, while mutations (T875R, D873E, T875R/D873E) repaired this interaction displayed opposite results. [2]更重要的是,JAK2 K607N 和突变破坏了这种相互作用,增强了 JAK2-STAT5 通路的激活和 Ba/F3 细胞的增殖。 [1] 突变(T875N、T875A、D873A 和 D873G)破坏了 T875 和 D873 的相互作用,增强了 JAK2 的活性,降低了其结构稳定性和 JH2 结构域的活性,进一步增强了 JAK2 的活性,而突变(T875R、D873E、T875R/D873E)修复了这种相互作用,显示相反结果。 [2]