学科主题临床医学
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
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
2015-07-01
DOI10.3109/10428194.2014.981177
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
WOS记录号WOS:000359888700038
项目编号30872923 ; RDB2007-47 ; RDK2008-01 ; RDB2011-25
资助机构National Natural Science Foundation of China ; Peking University People&prime ; s Hospital Research and Development Foundation
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55151
专题北京大学第二临床医学院_临床分子生物学研究所
北京大学第一临床医学院_眼科
北京大学第二临床医学院_血液科
北京大学第二临床医学院_医务处
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
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GB/T 7714
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.
APA Zuo, Bo.,Li, Mei.,Liu, Yulan.,Li, Kun.,Ma, Shuyun.,...&Yu, Weidong.(2015).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.LEUKEMIA & LYMPHOMA,56(7),2170-2181.
MLA Zuo, Bo,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".LEUKEMIA & LYMPHOMA 56.7(2015):2170-2181.
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