Ras Stabilization Through Aberrant Activation of Wnt/β-Catenin Signaling Promotes Intestinal Tumorigenesis

Woo-Jeong Jeong, Juyong Yoon, Jong-Chan Park, Soung-Hoon Lee, Seung-Hoon Lee, Saluja Kaduwal, Hoguen Kim, Jong-Bok Yoon, Kang-Yell Choi*

*To whom correspondence should be addressed. E-mail: kychoi{at}yonsei.ac.kr

This PDF file includes:

• Fig. S1. Role of GSK3β and Axin in the regulation of H-Ras stability.
• Fig. S2. H-Ras phosphorylation at Ser¹⁸³ is not involved in its degradation.
• Fig. S3. The role of β-TrCP in regulating the stability of K- and N-Ras.
• Fig. S4. Thr¹⁴⁴ and Thr¹⁴⁸ of H-Ras are phosphorylated by GSK3β and are involved in its degradation.
• Fig. S5. Effects of H-Ras stabilization through GSK3β-mediated phosphorylation on ERK pathway activation by EGF.
• Fig. S6. Subcellular localization of Ras and p-Ras.
• Fig. S7. GSK3β inhibits cellular proliferation and transformation induced by oncogenic Ras through phosphorylation and subsequent degradation of H-Ras.
• Fig. S8. Effects of APC upon degradation and polyubiquitylation of H-Ras by overexpression of GSK3β.
• Fig. S9. Effects of Wnt3a on the stability of β-catenin and Ras in RKO cells.
• Fig. S10. Immunohistochemical analyses of Apc^Min/+ and Apc^1638N mice.
• Fig. S11. Immunohistochemical and immunoblot analyses and mutational status of Apc and K-Ras genes of adenocarcinoma from FAP patients.
• Fig. S12. Specificity test for the antibody that detects phosphorylated Ras in immunohistochemical analyses.
• Fig. S13. DNA copy numbers of K-Ras, N-Ras, TOP1, and GAPDH in human colorectal adenocarcinoma.
• Fig. S14. mRNA expression of K-, N-, and H-Ras and PCNA in human colorectal adenoma.
  

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© 2012 American Association for the Advancement of Science