北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第二临床医学院  > 临床分子生物学研究所  > 期刊论文
学科主题: 临床医学
题名:
G-protein coupled receptor 34 activates Erk and phosphatidylinositol 3-kinase/Akt pathways and functions as alternative pathway to mediate p185Bcr-Abl-induced transformation and leukemogenesis
作者: Zuo, Bo1; Li, Mei1; Liu, Yulan1; Li, Kun1; Ma, Shuyun1; Cui, Meihua4; Qin, Yazhen2; Zhu, Honghu2; Pan, Xiuying1; Guo, Jingzhu3; Dai, Zonghan5; Yu, Weidong1
关键词: Leukemogenesis ; Gpr34 ; Bcr-Abl ; apoptosis ; PI3K/Akt pathway ; IL-3
刊名: LEUKEMIA & LYMPHOMA
发表日期: 2015-07-01
DOI: 10.3109/10428194.2014.981177
卷: 56, 期:7, 页:2170-2181
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology ; Hematology
研究领域[WOS]: Oncology ; Hematology
关键词[WOS]: CHRONIC MYELOID-LEUKEMIA ; BCR-ABL ; TYROSINE KINASE ; MALT LYMPHOMA ; EXPRESSION ; BCR/ABL ; APOPTOSIS ; CELLS ; MECHANISM ; GPR34
英文摘要:

Tyrosine 177 and the Src homology 2 (SH2) domain play important roles in linking p185Bcr-Abl to downstream pathways critical for cell growth and survival. However, a mutant p185(Y177FR552L) (p185(YR)), in which tyrosine 177 and arginine 552 in the SH2 domain are mutated, is still capable of transforming hematopoietic cells in vitro. Transplant of these cells into syngeneic mice also leads to leukemogenesis, albeit with a phenotype distinct from that produced by wild-type p185Bcr-Abl (p185(wt))-transformed cells. Here we show that G-protein coupled receptor 34 (Gpr34) expression is markedly up-regulated in p185(YR)-transformed cells compared to those transformed by p185(wt). Knockdown of Gpr34 in p185(YR) cells is sufficient to suppress growth factor-independent proliferation and survival in vitro and attenuate leukemogenesis in vivo. The Erk and phosphatidylinositol 3-kinase/Akt pathways are activated in p185(YR) cells and the activation is dependent on Gpr34 expression. These studies identify Gpr34 as an alternative pathway that may mediate p185Bcr-Abl-induced transformation and leukemogenesis.

语种: 英语
所属项目编号: 30872923 ; RDB2007-47 ; RDK2008-01 ; RDB2011-25
项目资助者: National Natural Science Foundation of China ; Peking University People&prime ; s Hospital Research and Development Foundation
WOS记录号: WOS:000359888700038
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55151
Appears in Collections:北京大学第二临床医学院_临床分子生物学研究所_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.Peking Univ, Peoples Hosp, Inst Clin Mol Biol, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Inst Hematol, Beijing 100044, Peoples R China
3.Peking Univ, Peoples Hosp, Dept Pediat, Beijing 100044, Peoples R China
4.Peking Univ, Aerosp Ctr Hosp, Dept Gastroenterol, Beijing 100044, Peoples R China
5.Texas Tech Univ, Hlth Sci Ctr, Dept Internal Med, Amarillo, TX USA

Recommended Citation:
Zuo, Bo,Li, Mei,Liu, Yulan,et al. G-protein coupled receptor 34 activates Erk and phosphatidylinositol 3-kinase/Akt pathways and functions as alternative pathway to mediate p185Bcr-Abl-induced transformation and leukemogenesis[J]. LEUKEMIA & LYMPHOMA,2015,56(7):2170-2181.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Zuo, Bo]'s Articles
[Li, Mei]'s Articles
[Liu, Yulan]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Zuo, Bo]‘s Articles
[Li, Mei]‘s Articles
[Liu, Yulan]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace