The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL.

MLA

Mian, A. A., et al. “The Gatekeeper Mutation T315I Confers Resistance against Small Molecules by Increasing or Restoring the ABL-Kinase Activity Accompanied by Aberrant Transphosphorylation of Endogenous BCR, Even in Loss-of-Function Mutants of BCR/ABL.” Leukemia (08876924), vol. 23, no. 9, Sept. 2009, pp. 1614–21. EBSCOhost, https://doi.org/10.1038/leu.2009.69.

APA

Mian, A. A., Schüll, M., Zhao, Z., Oancea, C., Hundertmark, A., Beissert, T., Ottmann, O. G., & Ruthardt, M. (2009). The gatekeeper mutation T315I confers resistance against small molecules by increasing or restoring the ABL-kinase activity accompanied by aberrant transphosphorylation of endogenous BCR, even in loss-of-function mutants of BCR/ABL. Leukemia (08876924), 23(9), 1614–1621. https://doi.org/10.1038/leu.2009.69

Chicago

Mian, A. A., M. Schüll, Z. Zhao, C. Oancea, A. Hundertmark, T. Beissert, O. G. Ottmann, and M. Ruthardt. 2009. “The Gatekeeper Mutation T315I Confers Resistance against Small Molecules by Increasing or Restoring the ABL-Kinase Activity Accompanied by Aberrant Transphosphorylation of Endogenous BCR, Even in Loss-of-Function Mutants of BCR/ABL.” Leukemia (08876924) 23 (9): 1614–21. doi:10.1038/leu.2009.69.