Lack of Bcl11b tumor suppressor results in vulnerability to DNA replication stress and damages

@article{Kamimura2007LackOB,
  title={Lack of Bcl11b tumor suppressor results in vulnerability to DNA replication stress and damages},
  author={Keisuke Kamimura and Yukio Mishima and Masanori Obata and Takao Endo and Yutaka Aoyagi and Ryo Kominami},
  journal={Oncogene},
  year={2007},
  volume={26},
  pages={5840-5850}
}
Bcl11b/Rit1 is involved in T-cell development and undergoes chromosomal rearrangements in human T-cell leukemias. Thymocytes of Bcl11b−/− newborn mice exhibit apoptosis at a certain developmental stage when thymocytes re-enter into the cell-cycle. Here, we show that Bcl11b-knockdown T-cell lines, when exposed to growth stimuli, exhibited apoptosis at the S phase with concomitant decreases in a cell-cycle inhibitor, p27 and an antiapoptotic protein, Bcl-xL, owing to transcriptional repression… CONTINUE READING

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