JAK2 is a constitutive protein tyrosine kinase (PTK) which can activate JAK-STAT signaling.
JAK2是一种组成性酪氨酸激酶，能激活JAK - STAT信号传导途径。
STAT proteins are activated by G-protein coupled receptors, while it has not been reported whether CCK receptors, a kind of G-protein coupled receptors, can activate JAK/STAT pathway.
STAT蛋白可被G 蛋白偶联受体激活，而CCK 受体作为一种G 蛋白偶联受体，是否对JAK／STAT通路具有直接激活作用，尚未见报道。
The JAK/STAT pathway that contributes to signal transduction by cytokines, growth factors and hormones is universally activated in leukemias.
JAK/S TAT通路是细胞因子、生长因子、激素等广泛应用的信号转导通路，白血病形成中普遍存在JAK/STAT通路的持续激活。
We incidentally found that STAT1C overexpression cause aberrant STAT activation in LL2 cells. Further studies on the underlying mechanisms may explore a novel regulatory system of JAK/STAT pathway.
我们偶然发现送入细胞内的STAT1C过量表现会造成LL2细胞异常的STAT蛋白活化，进一步研究其机制也许能发现一些新的JAK/STAT讯息传递路径的调节系统。
We incidentally found that STAT1C overexpression cause aberrant STAT activation in LL2 cells. Further studies on the underlying mechanisms may explore a novel regulatory system of JAK/STAT pathway.
我们偶然发现送入细胞内的STAT1C过量表现会造成LL2细胞异常的STAT蛋白活化，进一步研究其机制也许能发现一些新的JAK/STAT讯息传递路径的调节系统。
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