Supplementary Materials

Supplementary Materials for:

RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis

Peter S. Winter, Kristopher A. Sarosiek, Kevin H. Lin, Manja Meggendorfer, Susanne Schnittger, Anthony Letai, Kris C. Wood*

*Corresponding author. E-mail: kris.wood{at}

This PDF file includes:

  • Fig. S1. RAS effector pathway activation confers resistance to JAK inhibition in an additional JAK2V617F-positive cell line, Set2.
  • Fig. S2. Weak-scoring constructs from the primary screen—IKKα and Notch1—do not confer resistance to JAK inhibition in secondary GI50 assays.
  • Fig. S3. AKT-mediated resistance to JAK inhibition occurs independently of downstream mTOR activity.
  • Fig. S4. BH3 profiling of HEL92.1.7 derivatives shows similar mitochondrial priming that is independent of JAK inhibitor sensitivity.
  • Fig. S5. PIM1 and ERK phosphorylate BAD at Ser112 downstream of JAK/STAT signaling and influence subsequent entrance into apoptosis.
  • Fig. S6. BH3 profiling indicates that HMLE cells are not depolarized by BAD peptide and thus are not dependent on BCL-2/BCL-XL.
  • Fig. S7. An additional JAK2V617F-positive cell line, Set2, shows sensitivity to inhibition of BCL-XL, but not BCL-2.
  • Legends for tables S1 and S2
  • Table S3. List of hairpin sequences.
  • Legend for table S4

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Technical Details

Format: Adobe Acrobat PDF

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Other Supplementary Material for this manuscript includes the following:

  • Table S1 (Microsoft Excel format). List of pathway-activating constructs and controls.
  • Table S2 (Microsoft Excel format). Patient cohort information.
  • Table S4 (Microsoft Excel format). Primary screen data.

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Citation: P. S. Winter, K. A. Sarosiek, K. H. Lin, M. Meggendorfer, S. Schnittger, A. Letai, K. C. Wood, RAS signaling promotes resistance to JAK inhibitors by suppressing BAD-mediated apoptosis. Sci. Signal. 7, ra122 (2014).

© 2014 American Association for the Advancement of Science