期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

内皮和造血系统特异性敲除Rictor基因对胎肝造血的影响 被引量：1

Effect of Rictor Gene Deletion in Endothelial and Hematopoietic Cells on Fetal Liver Hematopoiesis
下载PDF
导出
摘要 目的:研究Rictor基因对胚胎发育过程中胎肝造血的影响。方法:利用Cre-LoxP基因敲除系统,特异性在小鼠内皮(VEC-Cre)和造血(Vav1-Cre)系统敲除Rictor基因;通过流式细胞术分析特异敲除Rictor基因后小鼠胚胎第15 d胎肝中的各系细胞比例的变化,并进一步分析造血干细胞的变化。结果:利用VEC-Cre和Vav1-Cre小鼠敲除Rictor基因后,胎肝中各系细胞比例均有所减少,B细胞比例的减少较为明显,造血干细胞比例也明显减少。结论:Rictor基因敲除损害胎肝组织中造血干细胞的产生和各系细胞的分化。 Objective： To study the role of Rictor gene in fetal liver hematopoiesis. Methods： Using Cre-LoxP knockout system（endothelial VEC-Cre and hematopoietie Vavl-Cre）, we specifically deleted Rictor gene in mouse endothelial cells or hematopoietic cells, to analyze the influence of Rictor-deletion on B cells, T cells, bone marrow myeloid cells and hematopoietic stem cells（HSC） in E15 fetal liver by fluorescence activated cell sortor. Results： Rictor-deletion by VEC-cre or Vavl-cre mice leads to a significant decrease in B cells, T cells, GM cells and HSC in E15 fetal liver, especially for the reduction in B cells population respectively. Conclusion： Rictor-deletion causes impairment of HSC proliferation and lineage cell differentiation in E15 fetal liver.
作者 穆晓环 王伟丽 赵云泽 倪艳丽 李专 顾洁 张丽艳 汪晓敏 程涛 刘汉芝 袁卫平 刘兵
机构地区 中国医学科学院&北京协和医学院血液学研究所血液病医院实验血液学国家重点实验室 军事医学科学院附属医院肿瘤学研究室
出处 《生物技术通讯》 CAS 2014年第3期310-315,共6页 Letters in Biotechnology
基金 国家重点基础研究发展计划(2012CB966604 2011CB964800 2013CB966902) 国家自然科学基金(81090414 81330015 81130074 81070390 81300436)
关键词 Rictor基因 VEC-Cre Vav1-Cre 胎肝造血 哺乳动物雷帕霉素靶蛋白 Rictor gene VEC-Cre Vavl-Cre fetal liver hematopoiesis mammalian target of rapamycin
分类号 Q25 [生物学—细胞生物学] Q78 [生物学—分子生物学]
  • 相关文献

参考文献14

  • 1Sabatini D M. mTOR and cancer: insights into a complex rela- tionship[J]. Nat Rev Cancer, 2006,6:729-734.
  • 2Zoncu R, Efeyan A, Sabatini D M. mTOR: from growth sig- nal integration to cancer, diabetes and ageing[J]. Nat Rev Mol Cell Biol, 2011,12:21-35.
  • 3Kumar A, Harris T E, Keller S R, et al. Muscle-specific de- letion of Rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity[J]. Mol Cell Bi- ol, 2008,28:61-70.
  • 4Xu Q, Simpson S E, Scialla T J, et al. Survival of acute my-eloid leukemia cells requires PI3 kinase activation[J]. Blood, 2003,102:972-980.
  • 5Muller A M, Medvinsky A, Strouboulis J, et al. Development of hematopoietic stem cell activity in the mouse embryo~J]. Immunity, 1994,1:291-301.
  • 6Li Z, Lan Y, He W, et al. Mouse embryonic head as a site for hematopoietic stem cell development[J]. Cell Stem Cell, 2012,11:663-675.
  • 7Samokhvalov I M, Samokhvalova N I, Nishikawa S. Cell trac- ing shows the contribution of the yolk sac to adult haemato- poiesis[J]. Nature, 2007,446:1056-1061.
  • 8Cumano A, Godin I. Ontogeny of the hematopoietic system[J]. Annu Rev Immunol, 2007,25:745-785.
  • 9Zovein A C, Hofmann J J, Lynch M, et al. Fate tracing re- veals the endothelial origin of hematopoietic stem cells[J]. Cell Stem Cell, 2008,3:625-636.
  • 10Chen M J, Yokomizo T, Zeigler B M, et al. Runxl is re- quired for the endothelial to haematopoietic cell transition but not thereafter[J]. Nature, 2009,457:887-891.

二级参考文献12

  • 1Osaki M,Oshimura M,Ito H,et al.PI3K/AKT pathway:its func-tions and alterations in human cancer.Apoptosis,2004;9(6):667-676.
  • 2Livak KJ,Schmittgen TD.Analysis of relative gene expression datausing real-time quantitative PCR and the 2(-Delta Delta C(T))Method.Methods,2001;25(4):402-408.
  • 3Karoui M,Tresallet C,Julie C,et al.Loss of heterozygosity on 10qand mutational status of PTEN and BMPR1A in colorectal primarytumours and metastases.Br J Cancer,2004;90(6):1230-1234.
  • 4Nassif NT,Lobo GP,Wu X,et al.PTEN mutations are common insporadic microsatellite stable colorectal cancer.Oncogene,2004;23(2):617-628.
  • 5Colakoglu T,Yildirim S,Kayaseleuk F,et al.Clinicopathologicalsignificance of PTEN loss and the phosphoinositide 3-kinase/Aktpathway in sporadic colorectal neoplasms:is PTEN loss predictor oflocal recurrence?Am J Surg,2008;195(6):719-725.
  • 6Manning BD,Cantley LC.AKT/PKB signaling:navigating down-stream.Cell,2007;129(7):1261-1274.
  • 7Cheng GZ,Park S,Shu S,et al.Advances of AKT pathway in hu-man oncogenesis and as a target for anti-cancer drug discovery.CurrCancer Drug Targets,2008;8(1):2-6.
  • 8Sabatini DM.mTOR and cancer:insights into a complex relation-ship.Nat Rev Cancer,2006;6(9):729-734.
  • 9Campbell RA,Bhat-Nakshatri P,Patel NM,et al.Phosphatidylinos-itol 3-kinase/AKT-mediated activation of estrogen receptor alpha:anew model for anti-estrogen resistance.J Biol Chem,2001;276(13):9817-9824.
  • 10Brunet A,Bonni A,Zigmond MJ,et al.Akt promotes cell survivalby phosphorylating and inhibiting a Forkhead transcription factor.Cell,1999;96(6):857-868.

共引文献9

同被引文献2

引证文献1

生物技术通讯
2014年 第3期

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部