Present address: Department of Urology, Charité– Universitätsmedizin Berlin, Campus Charité Mitte, Charitéplatz 1, 10117 Berlin, Germany.
Tumor suppressor p16INK4a controls oncogenic K-Ras function in human pancreatic cancer cells
Version of Record online: 15 DEC 2011
© 2011 Japanese Cancer Association
Volume 103, Issue 2, pages 169–175, February 2012
How to Cite
Rabien, A., Sanchez-Ruderisch, H., Schulz, P., Otto, N., Wimmel, A., Wiedenmann, B. and Detjen, K. M. (2012), Tumor suppressor p16INK4a controls oncogenic K-Ras function in human pancreatic cancer cells. Cancer Science, 103: 169–175. doi: 10.1111/j.1349-7006.2011.02140.x
- Issue online: 1 FEB 2012
- Version of Record online: 15 DEC 2011
- Accepted manuscript online: 2 NOV 2011 11:06AM EST
- (Received May 25, 2011/Revised October 13, 2011/Accepted October 28, 2011/Accepted manuscript online November 2, 2011)
Fig. S1. The half-life of K-Ras is shortened by p16 re-expression in Capan-1 cells.
Fig. S2. K-Ras activity was significantly reduced in Capan-1 cells after transfection of human K-rasV12 antisense oligonucleotides.
Fig. S3. K-Ras and p16 seem to interact directly.
Fig. S4. p16 inhibits K-Ras activity in MiaPaCa-2 pancreatic cancer cells.
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