The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia.

@article{Espinosa2010TheNP,
  title={The Notch/Hes1 pathway sustains NF-κB activation through CYLD repression in T cell leukemia.},
  author={L. Manzano Espinosa and S{\'e}verine Cathelin and Teresa D'altri and Thomas Trimarchi and Alexander Statnikov and Jordi Guiu and Ver{\'o}nica Rodilla and Julia Ingl{\'e}s-Esteve and Josep Nomdedeu and Beatriz Bellosillo and Carlos Besses and O. A. L. Abdel-Wahab and Nicole Kucine and Shao-cong Sun and Guangchan Song and Charles Mullighan and Ross L. Levine and K. Rajewsky and Iannis Aifantis and Anna Bigas},
  journal={Cancer cell},
  year={2010},
  volume={18 3},
  pages={268-81}
}
It was previously shown that the NF-κB pathway is downstream of oncogenic Notch1 in T cell acute lymphoblastic leukemia (T-ALL). Here, we visualize Notch-induced NF-κB activation using both human T-ALL cell lines and animal models. We demonstrate that Hes1, a canonical Notch target and transcriptional repressor, is responsible for sustaining IKK activation in T-ALL. Hes1 exerts its effects by repressing the deubiquitinase CYLD, a negative IKK complex regulator. CYLD expression was found to be… CONTINUE READING

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