|
|
国际病理 2008, 28(2) 15-160 DOI:
ISSN: 0412-1961 CN: 21-1139/TG |
|
|
|
|
本期目录 |
下期目录 |
过刊浏览 |
高级检索
[打印本页]
[关闭]
|
|
| 综述 |
|
|
SOCS3与BCR-ABL阴性的骨髓增殖性疾病 |
|
|
王冬梅1;潘崚2 |
|
|
1.哈励逊国际和平医院血液科,河北衡水 053000; 2.河北医科大学第二医院血液科,石家庄 050000 |
|
|
摘要：
一系列细胞因子通过JAK/STAT通路诱导细胞因子信号转导抑制因子(SOCS)基因的表达，SOCS蛋白又负反馈调节细胞因子信号转导通路， 形成细胞因子信号转导反馈调节环。在BCR-ABL阴性的骨髓增殖性疾病的发病机制中，JAK2V617F点突变的发现是一个重大的突破。JAK2V617F点突变可导致SOCS3基因表达的增高，但通过某种机制逃逸了SOCS3的负向调控作用。 |
|
|
关键词：
细胞因子信号转导抑制因子
细胞因子信号转导通路
JAK/STAT通路
骨髓增殖性疾病
|
|
|
SOCS3 and BCR-ABL fusion gene negative myeloproliferative diseases |
|
|
WANG Dong-mei1, PAN Ling2
|
|
|
1.Department of Hemotology, Harrison International Peace Hospital,Hengshui Hebei 053000;
2.Department of Hemotology, Second Hospital of Hebei Medical University, Shijiazhuang 050000,China
|
|
|
Abstract:
Several cytokines induce the expression of the suppressor of cytokine signaling（SOCS）gene through JAK/STAT pathway, while SOCS protein negatively regulates signal transduction of cytokine pathway, and a negative feedback loop of cytokine signal transduction is thus completed. In BCR-ABL fusion gene negative myeloproliferative diseases，the discovery of JAK2V617F point mutation is an important landmark. Recently，it was demonstrated that JAK2V617F point mutation accompanied with highexpression of SOCS3. However, it is not clear why JAK2V617F mutant could escape the negative regulation by suppressor of cytokine signaling 3 in some of MPD patients. |
|
|
Keywords:
suppressor of cytokine signaling-3 (SOCS3)
signal transduction pathway
JAK/STAT pathway
myeloproliferative diseases
|
|
|
收稿日期 2007-09-14 修回日期 2007-10-22 网络版发布日期 |
|
|
DOI: |
|
|
基金项目:
|
|
|
通讯作者: 潘崚 |
|
|
作者简介: |
|
作者Email: |
|
|
| 参考文献： |
|
| 本刊中的类似文章 |
|
| 文章评论 |
|
|
|
| Copyright by 国际病理 |
