STK33 kinase is not essential in kras-dependent cells - Response

Cancer Research

Volumn 71, Issue 24, 2011, Pages 7717-

  Dussault, Isabelle ^a   Carnahan, Josette ^a   Babij, Carol ^a   Zhang, Yihong ^a   Watson, Vivienne J ^a   Quon, Kim ^a   Kassner, Paul D ^a  

^a AMGEN INC   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

K RAS PROTEIN; PROTEIN KINASE; PROTEIN KINASE INHIBITOR; PROTEIN STK33; SHORT HAIRPIN RNA; SMALL INTERFERING RNA; STK33 KINASE INHIBITOR; UNCLASSIFIED DRUG;

ACUTE GRANULOCYTIC LEUKEMIA; CANCER CELL; CANCER CELL CULTURE; CELL SURVIVAL; CELL VIABILITY; ENZYME ACTIVITY; LETTER; LEUKEMIA CELL; MUTANT; NEOPLASM; PRIORITY JOURNAL;

EID: 84255170347     PISSN: 00085472     EISSN: 15387445     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-11-3068     Document Type: Letter

References (4)

1. Babij C, Zhang Y, Kurzeja RJ, Munzli A, Shehabeldin A, Fernando M, et al. STK33 kinase activity is nonessential in KRAS-dependent cancer cells. Cancer Res 2011;71:5818-26.
2. Scholl C, Frohling S, Dunn IF, Schinzel AC, Barbie DA, Kim SY, et al. Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells. Cell 2009;137:821-34.
3. Barbie DA, Tamayo P, Boehm JS, Kim SY, Moody SE, Dunn IF, et al. Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature 2009;462:108-12.
4. Luo J, Emanuele MJ, Li D, Creighton CJ, Schlabach MR, Westbrook TF, et al. A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene. Cell 2009;137:835-48.