Conclusion JAK2 exon 12 mutations could exist in JAK2V617F-negative PV patients.
结论JAK2V 617 F点突变阴性的PV患者中存在JAK2外显子12突变。
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。
The tyrosine phosphorylated 130000 protein was identified as JAK2, a non receptor tyrosine kinase.
鉴定了分子量为130000酪氨酸磷酸化的蛋白质为JAK2，一种非受体型酪氨酸激酶。
There is high frequency of JAK2 V617F mutation in myeloproliferative disorders and it could be used as the diagnostic marker for myeloproliferative disorders.
JAK2基因V617F突变在骨髓增殖性疾病中有较高的检出率，可作为骨髓增殖性疾病特异性诊断指标。
The mechanism of action may be related to the decreased expression of JAK2 and STAT3 of hepatic tissue and blocking of JAK2/STAT3 signal transduction pathway.
肝复康对肝纤维化有疗效，其作用机制可能与降低肝组织JAK2和STAT3的表达，阻断JAK2/STAT3信号通路有关。
Methods Polymerase chain reaction(PCR)was used for 12 JAK2V617F -negative PV patients to amply the region of JAK2 exon 12, direct gene sequencing was performed to detect mutations of JAK2 exon 12.
方法采用聚合酶链反应（PCR）扩增12例JAK2V617F点突变阴性PV患者的JAK2外显子12片段，经基因测序与野生型JAK2外显子12比对，了解是否存在JAK2外显子12突变。
Methods Polymerase chain reaction(PCR)was used for 12 JAK2V617F -negative PV patients to amply the region of JAK2 exon 12, direct gene sequencing was performed to detect mutations of JAK2 exon 12.
方法采用聚合酶链反应（PCR）扩增12例JAK2V617F点突变阴性PV患者的JAK2外显子12片段，经基因测序与野生型JAK2外显子12比对，了解是否存在JAK2外显子12突变。
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