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甲异靛对K562细胞的作用及其机制的初步研究 被引量:10

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出处 《中华血液学杂志》 CAS CSCD 北大核心 2004年第1期43-45,共3页 Chinese Journal of Hematology
基金 国家自然科学基金资助项目 (3 9870 773 )
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参考文献6

  • 1Sonoyama J,Matsumura I,Ezoe S,et al.Functional of cooperation among Ras, STAT5, and phosphatidylinositol 3-kinase is required for full oncogenic activities of BCR-ABL in K562[].Journal of Biological Chemistry.2002
  • 2de Groot RP,Raaijmakers JAM,Lammers JW,et al.STAT5 activation by BCR-ABL contributes to transformation of K562 leukemia cells[].Blood.1999
  • 3Kang CD,Yoo SD,Hwang BW,et al.The inhibition of ERK MAPK not the activation of JNK SAPK is primary required to induce apoptosis in chronic myelogenous leukemia K562 cells[].Leukemia Research.2000
  • 4Gesbert F,Griffin JD.Bcr Abl activates transcription of the bcl-x gene through STAT5[].Blood.2000
  • 5Xiao ZJ,Qian LS,Liu BC,et al.Meisoindigo for the treatment of chronic myelogenous leukemia[].British Journal of Haematology.2000
  • 6Neshat MS,Raitano AB,Wang HG,et al.The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and independent pathways: roles for phosphatidylinositol 3-kinase and Raf[].Molecular and Cellular Biology.2000

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