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  • 标题:Thymic tumorigenesis induced by overexpression of p56lck.
  • 本地全文:下载
  • 作者:K M Abraham ; S D Levin ; J D Marth
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:1991
  • 卷号:88
  • 期号:9
  • 页码:3977-3981
  • DOI:10.1073/pnas.88.9.3977
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:The lck gene encodes a membrane-associated protein tyrosine kinase (p56lck) that is believed to participate in lymphocyte-specific signal transduction pathways. To investigate the function of this molecule, transgenic mice were generated carrying the wild-type lck gene or a mutated lck gene encoding a constitutively activated form of p56lck (p56lckF505). Transgene expression in thymocytes was achieved in each case using the lck proximal promoter element. Mice expressing high levels of either p56lckF505 or p56lckY505 reproducibly developed thymic tumors. The sensitivity of thymocytes to p56lck-induced transformation suggests that disturbances in lck expression may contribute to the pathogenesis of some human neoplastic diseases.
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