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Hct116 p53−/−

WebTreatment 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 … 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 …

p53 transcriptionally regulates SQLE to repress ... - EMBO Press

WebLanguage Label Description Also known as; English: HCT 116 TP53(-/-) cell line 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−/− cells, and of Bax+/− and Bax−/− cells. We identify a novel proapoptotic function of p53 that does not require activation by genotoxic agents and that appears to be constitutively … heartland swift current https://louecrawford.com

Hsp27 Modulates p53 Signaling and Suppresses Cellular Senescence

WebAug 28, 2024 · The HCT116 p53−/− cell line was generated in our lab. HCT116 p53−/− and HCT116 p53 endogenous point mutant cell lines were cultured in Iscove’s Modified Dulbecco’s Medium (HyClone, USA) with 10% fetal bovine serum (FBS, Gibco, USA) and 1% penicillin/streptomycin (Gibco, USA). When cells reached 80–90% confluence, cell … WebTo establish p53 dependence more clearly, we compared protein levels from HCT116 wt and HCT116 p53 −/− cells, following D4476 treatment (Fig. 5, B and C). In HCT116 wt … WebIdentification of ASS1 as a direct target of p53. (A) Schematics of the integrated OMICS approach. HCT116 p53 +/+ and HCT116 p53 −/− cells were treated with ADR (2 mg/ml) for 2 hours and... heartland sweetheart wood stove

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Hct116 p53−/−

Redefining the p53 response element PNAS

WebMay 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 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 …

Hct116 p53−/−

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WebFeb 27, 2004 · Exogenous p53 Responds to DNA Damage in p53 Knockout HCT116 Cells—Wild type p53 was cloned into a lentiviral vector under the control of the RSV … WebThere 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.

WebApr 13, 2024 · HCT116, HCT116 p53 −/−, and HCT116-5FUR cells were treated with mannose (50 mM) and 5-FU (5 μM) alone or in combination for up to 72 h. Cells treated … WebApr 13, 2024 · HCT116, HCT116 p53 −/−, and HCT116-5FUR cells were treated with mannose (50 mM) and 5-FU (5 μM) alone or in combination for up to 72 h. Cells treated with mannose/5-FU showed a significant cell accumulation in the sub-G 1 region in a time-dependent manner in HCT116 and HCT116 p53 −/− but not in HCT116-5FUR cells ( …

WebJan 2, 2024 · To further confirm the effect of MARCH7 on cell proliferation is mediated by p53, the paired HCT116 cell lines (p53 +/+ and p53 −/−) were used. Knockdown of MARCH7 markedly inhibited the proliferation of HCT116 p53 +/+ cells, but not HCT116 p53 −/− cells (Fig 6B, Appendix Fig S5D). To determine whether the effect of MARCH7 on …

WebThere 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 …

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 ... mount rogers careersWebJul 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 … mount rock north carolinaWebNov 12, 2015 · In addition, in response to DNA damage, p53 induced FTH1 and suppressed transferrin receptor, which regulates iron entry into cells. HCT116 p53+/+ cells were resistant to iron accumulation,... mount rogers community services board careersWebCollateral sensitivity of the resistant HCT116 p53− /− colon adenocarcinoma cells to SCHL was observed as well as the normal sensitivity of CEM/ADR5000 leukemia cells, MDA-MB-231-BCRP breast adenocarcinoma cells and U87. MGΔEGFR glioblastoma cells. SCHL induced apoptosis in CCRF-CEM cells via caspases 3/7-, 8- and 9-activation, MMP ... mount rock ncWebFor 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 mountrock リュックWebAug 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 … mount rock paWebIt is shown that tumor suppressor protein p53 accumulate in this pathway. We further compared WT and p53−/− HCT116 and found that p53−/− HCT116 is more resistant to aciculatin. The same results can be achieved by knockdown of p53 level in WT cells. These data suggest that p53 plays a crucial role in aciculatin‐induced apoptosis. heartland swift current sk