Hct116 p53−/−
WebJan 12, 2024 · Wild-type HCT116 cells (HCT116/p53 +/+) and p53 knockout HCT116 cells (HCT116/p53 −/−) were a gift from Dr. Yao Lin (Fujian Normal University, Fujian, China) … WebAbstract. To dissect apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence Bcl-2 and Bcl-x L in isogenic clones of p53+/+ and p53−/− …
Hct116 p53−/−
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WebJul 26, 2013 · HCT116 cells were treated with 26 μM ALLN for 24 h; significant cell death was detected in the HCT116 cells and HCT116/p53 −/− cells, but was inhibited in HCT116/Bax −/− cells (Fig. 3 B). Decreased pro-caspase-3 and cleaved PARP were seen in ALLN-treated HCT116 cells and HCT116/ p53 −/− cells, but pro-caspase-3 remained … WebDec 2, 2005 · Moreover, similar results were obtained with HCT116 parental cells (wt p53) versus the p53 somatic KO isogenic cells when treated with genotoxic agents. ... The −162/−116 sequence of the Rad51 promoter is shown with quarter sites in the p53-binding consensus (Rad51-1) ...
WebDownload scientific diagram Influence of PHA680632 on cell cycle in p53wt vs p53−/− HCT116 cells. (A and B) analysis of the cell cycle. (A) Quantitative data of cell cycle distribution after ... WebFor the first time, the pharmacokinetic (PK) profile of tryptophanol-derived isoindolinones, previously reported as p53 activators, was investigated. From the metabolites’ identification, performed by liquid chromatography coupled to high resolution
WebProliferation of HCT116 (p53+/+) cells after Siva-1 knockdown has been found lower than in HCT116 (p53−/−) cells, suggesting that Siva-1 still enhances cell proliferation in a p53-dependent manner. Possibly through the suppression of the p53 protein level, ... WebFeb 7, 2024 · D-(i) Western blot analysis of the depletion efficiency of RNF8 and p53 in differently treated HCT116 cells. (ii) CCK-8 experiment shows that the proliferation ability of differently treated cells. HCT116 WT-shCTR, HCT116 WT-shRNF8 and HCT116 p53−/−-shRNF8 cells were treated with DMSO, 10 or 30 μmol/L Eto for 20 min and then …
WebN = 3 ± SEM. (B) Quantitative RT-PCR analysis of p53 transcriptional targets in HCT116 p53 +/+ and p53 −/− cells. The analysis was performed 6 days post-transduction with …
WebMar 24, 2004 · Abstract. To elucidate mechanisms of resistance to chemotherapies currently used in the first-line treatment of advanced colorectal cancer, we have developed a … ccu school of businessWebMay 28, 2012 · HCT116 p53 wildtype cells died significantly more than HCT116 p53−/− cells with 3 and 5 mg/ml at both time points, 24 h (26% versus 40% respectively) and at 48 h (14% versus 28%, respectively) (p < 0.05). Saffron induces a p53-dependent cell cycle arrest in HCT116 cells ccusd boardWebMay 28, 2012 · This is the first study showing the effect of saffron in HCT116 colorectal cancer cells with different p53 status. Saffron induced DNA-damage and apoptosis in … ccu school scheduleWebTreatment of HCT116 cells with 200 ng/ml nocodazole induced a much stronger apoptotic response in p53+/+ cells than in p53−/− cells. As shown in Fig. 1, endonucleolytic … butchers rydeWebAug 25, 2009 · The use of p53-specific siRNA in HCT116 (p53 +/+) cells also elicited the same divergent pattern of p53 transcriptional behavior, where Lasp1 mRNA was up … ccus cluster sequencing consultationWebOct 28, 2003 · N, input, or total chromatin sample; Ab+, samples immunoprecipitated with p53 antibody; Ab−, mock immunoprecipitation control without p53 antibody. HCT116 p53−/− cells were used as a negative p53 binding control. p21primers flanking a well-documented p53 consensus site were used as a positive binding control. The input PCR signal was … ccus clean energyWebThere was no increase in cell death in the untreated or DMSO-treated cells. The rate of cell death after treatment with 10 or 11 was similar in HCT116 and HCT116p53 −/− (only slightly lower in p53-deficient cells exposed to 10 for 72, p < 0.05, Figure 4g) and significantly increased starting at 24 or 36 h for 10 and 11, respectively. ccusd93 powerschool