Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits Leukemogenesis

@inproceedings{Grebien2011TargetingTS,
  title={Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits Leukemogenesis},
  author={Florian Grebien and Oliver Hantschel and John Wojcik and Ines Kaupe and Boris Kovacic and Arkadiusz M. Wyrzucki and Gerald D. Gish and Sabine Cerny-Reiterer and Akiko Koide and Hartmut Beug and Tony J. Pawson and Peter Valent and Shohei Koide and Giulio Superti-Furga},
  booktitle={Cell},
  year={2011}
}
Chronic myelogenous leukemia (CML) is caused by the constitutively active tyrosine kinase Bcr-Abl and treated with the tyrosine kinase inhibitor (TKI) imatinib. However, emerging TKI resistance prevents complete cure. Therefore, alternative strategies targeting regulatory modules of Bcr-Abl in addition to the kinase active site are strongly desirable. Here, we show that an intramolecular interaction between the SH2 and kinase domains in Bcr-Abl is both necessary and sufficient for high… CONTINUE READING
Recent Discussions
This paper has been referenced on Twitter 10 times over the past 90 days. VIEW TWEETS

Citations

Publications citing this paper.
Showing 1-10 of 46 extracted citations

References

Publications referenced by this paper.
Showing 1-10 of 38 references

Similar Papers

Loading similar papers…