Binding of FLT3L to its cognate tyrosine kinase receptor, FLT3, activates STAT3 and STAT5 (1, 3).
FLT3L结合到与它同源的酪氨酸激酶的受体FLT3结合激活STAT3和STAT 5 (1,3)。
Secondary FLT3-TKD mutations are associated with treatment failure with tyrosine kinase inhibitors.
继发性FLT3 - TKD突变与酪氨酸激酶抑制剂治疗失败有关。
We investigated the effects and mechanisms of Flt3 signaling and 4-1bbl reverse signaling to monocytes.
同时还探讨了4 - 1bbl逆向信号对单核细胞的作用及可能的机理。
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