Supplementary Materials

Supplementary Materials for:

A Kinase-Independent Role for Unoccupied Insulin and IGF-1

Receptors in the Control of Apoptosis

Jeremie Boucher, Yazmin Macotela, Olivier Bezy, Marcelo A. Mori, Kristina Kriauciunas, C. Ronald Kahn*

*To whom correspondence should be addressed. E-mail: c.ronald.kahn{at}joslin.harvard.edu

This PDF file includes:

  • Fig. S1. Insulin signaling and growth rate in wild-type and DKO cells.
  • Fig. S2. DKO cells show reduced cytochrome c release from mitochondria but no difference in mitochondrial mass.
  • Fig. S3. Reduced apoptosis in DKO cells.
  • Fig. S4. Abundance of proteins involved in apoptosis in wild-type and DKO cells.
  • Fig. S5. mRNA abundance of proteins involved in apoptosis in wild-type and DKO cells.
  • Fig. S6. Abundance of apoptotic proteins in control and DKD MEFs.
  • Fig. S7. Bcl-2, Bax, and Flip abundance in IRKO and IGFRKO cells.
  • Fig. S8. Bax, Bcl-2, and Bcl-xL abundance in DKO cells expressing IR, IGF1R, or an inactive IR mutant.
  • Fig. S9. Effect of inhibition or activation of insulin signaling on caspase 3 cleavage and Bax, Bcl-2, and Flip abundance in wild-type cells.

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Citation: J. Boucher, Y. Macotela, O. Bezy, M. A. Mori, K. Kriauciunas, C. R. Kahn, A Kinase-Independent Role for Unoccupied Insulin and IGF-1 Receptors in the Control of Apoptosis Sci. Signal.3, ra87 (2010).

© 2010 American Association for the Advancement of Science