Supplementary Materials for:
The VDAC2-BAK Rheostat Controls Thymocyte Survival
Decheng Ren, Hyungjin Kim, Ho-Chou Tu, Todd D. Westergard, Jill K. Fisher, Jeff A.
Rubens, Stanley J. Korsmeyer, James J.-D. Hsieh, Emily H.-Y. Cheng*
*To whom correspondence should be addressed. E-mail:
This PDF file includes:
- Fig. S1. VDAC1 and VDAC2 are found in a wide range of mouse tissues.
- Fig. S2. Abundance of VDAC2 by genotype.
- Fig. S3. Analysis of thymocyte numbers by genotype.
- Fig. S4. Effect of the deficiency in Vdac2 on the abundance of other VDAC isoforms and of pro- and antiapoptotic proteins.
- Fig. S5. Conditional deletion of Vdac2 results in enhanced apoptosis in DP thymocytes.
- Fig. S6. WT and Vdac2 null thymocytes display comparable kinetics of BIM
- Fig. S7. Deficiency in Bak rescues the apoptotic phenotype associated with deletion
- Fig. S8. Deficiency in Bax fails to rescue the apoptotic phenotype associated with
deletion of Vdac2.
- Fig. S9. Deficiency in both Vdac2 and Bak does not affect homeostasis or survival of
- Fig. S10. Vdac2 null thymocytes display an enhanced apoptotic response to TCR
stimulation, which is rescued by deficiency in Bak, but not Bax.
- Fig. S11. PCR analysis of Vdac2 deletion in thymocyte subsets.
Format: Adobe Acrobat PDF
Size: 2.6 MB
D. Ren, H. Kim, H.-C. Tu, T. D. Westergard, J. K. Fisher, J. A. Rubens, S. J.
Korsmeyer, J. J.-D. Hsieh, E. H.-Y. Cheng, The VDAC2-BAK rheostat controls thymocyte
survival. Sci. Signal. 2, ra48 (2009).
© 2009 American Association for the Advancement of Science