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This study investigates the impact of CG200745 and SAHA on histone acetylation and key tumor suppressor proteins in RKO cells. Specifically, it examines the acetylation levels of histone H3 and p53, along with the expression of p21Waf1/Cip1, Mdm2, and β-actin, under various treatment conditions. Results showed significant alterations in protein levels over time with implications for cancer therapy strategies. The study utilized immunoblotting and quantification methods to analyze the protein interactions and acetylation states.
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Fig. 1 a b 0 0.5 1 2 4 8 16 24 (h) - + + + + + + + CG200745 Acetyl-histone H3 β-actin c - (µM) 0.1 1 10 CG200745 SAHA Acetyl-histone H3 β-actin
Fig. 2 a 4 8 16 24 16 (h) 0 1 2 - + + + + + + CG200745 SAHA p53 Mdm2 p21Waf1/Cip1 β-actin b c
Fig. 3 a b * *p<0.05 *p<0.05 * * * * * RKO RKO RC10.1 RC10.1
Fig. 4 a 8hr+CHX+CG200745 8hr+CHX 5 0 5 10 20 40 60 0 10 20 40 60 (min) p53 β-actin b 8hr+CHX+CG200745 8hr+CHX
Fig. 5 a 0 1 2 4 8 16 24 (hr) 16 + + + + + - + IgG Input SAHA CG200745 IB: Ac-p53(K320) IB: Ac-p53(K373) IP: p53 IB: Ac-p53(K382) IB: p53 b p53 mutants Vector C p53 WT K320R K373R K382R p53 β-actin
Fig. 5 (continued) No treatment c CG200745 (10 μM) K320R K373R K382R C p53 WT p53 mutants
Fig. 6 No treatment CG200745 (10 μM) K320R K373R K382R C p53 WT p53 mutants
Supplementary Fig. 1 a K320R K373R K382R K320R K382R K373R K382R K320R K373R p53 WT vector K373R K382R C K320R p53 WT CG200745 p53 - - - - - - - - - - - Mdm2 + + + + + + + + + + + p21Waf1/Cip1 β-actin c b K320R K320R K373R K373R K382R K382R C p53 WT p53 mutants Vector Vector p53 mutants C p53 WT
