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SUPPLEMENTARY DATA
Temporal and differential regulation of KAISO-controlled transcription by phosphorylated and acetylated p53 highlights a crucial regulatory role of apoptosis
Seo-Hyun Choi, Dong-In Koh, Su-Yeon Cho, Min-Kyeong Kim, Kyung-Sup Kim, and Man-Wook Hur*
Brain Korea 21 Plus Project for Medical Sciences, Department of Biochemistry and Molecular Biology, Severance Biomedical Research Institute, Yonsei University
School of Medicine, 50-1 Yonsei-Ro, SeoDaeMoon-Ku, Seoul 03722, Korea
*To whom correspondence may be addressed: Man-Wook Hur, Department of Biochemistry and Molecular Biology, Yonsei University School of Medicine, 134, ShinChon-Dong, SeoDaeMoon-Ku, Seoul, Korea 120-752, Tel: 82-2-2228-1678, Fax: 82-2-312-5041; E-mail: [email protected]
SUPPLEMENTARY FIGURES
Supplementary Figure 1. Induction of KAISO expression by other DNA damaging
reagents is p53-dependent. (A, B) RT-qPCR and western blot analysis of KAISO and p53
expression. HCT116 p53+/+, HCT116 p53-/- cells were treated with cisplatin (20 µM) or 5-FU (50
µM) harvested at the indicated times, and analyzed for mRNA by RT-qPCR, and protein
expression by western blot analysis, respectively. GAPDH, control.
Supplementary Figure 2. KAISO induces apoptosis only in wild type p53-expressing in
H1299 cells. (A) Flow cytometry analysis. The SNU61, Colo320DM, LS1034, HT-29 cells
expressing endogenous p53 “hot spot” mutant was transfected with KAISO expression or
control vector and were stained with propidium iodide and annexin V, using and apoptosis
detection kit (BD Bioscience). (B) Flow cytometry analysis of apoptosis of H1299 p53-null
cells transfected with KAISO, WT p53, p53R175H, p53G245S, p53R248W, and p53R273H
expression vector in the combination indicated.
