Hct116 p53+/+
WebIn summary, p53-null HCT116 cells transduced with a lentiviral vector expressing wild type p53 respond to DNA-damaging and … WebJan 17, 2006 · This analysis was based on a combination of denaturing HPLC mutation screening of all exons of the p53 gene, sequencing the cDNA, and assessing the …
Hct116 p53+/+
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WebMar 15, 2004 · To elucidate mechanisms of resistance to chemotherapies currently used in the first-line treatment of advanced colorectal cancer, we have developed a panel of HCT116 p53 wild-type (p53 (+/+)) and null (p53 (-/-)) isogenic colorectal cancer cell lines resistant to the antimetabolite 5-fluorouracil (5-FU), topoisomerase I inhibitor irinotecan … WebTherefore, HCT116 p53+/+ cells are simply marked as HCT116 except for in Figure 1. Our results confirmed that ES induced apoptosis by reducing the expression of c-Myc and …
WebApr 7, 2024 · E-cadherin and vimentin staining of metastatic tumors in the livers ( G) and lungs ( H) with HCT116-sh-DDX21 and HCT116-sh-NC cells. Scale bar stands for 50 μm length. The protein expression...
WebJul 20, 2024 · Comparable radiosensitivities of p53 +/+ and p53-/-HCT116 colorectal cells induced by CIR were demonstrated, as well as persistent 53BP1 foci indicated DNA repair deficiency in both cell lines. Different degree of premature senescence in isogenic HCT116 colorectal cancer cells suggested that CIR-induced premature senescence was more … 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-regulated to 154%, whereas p21 mRNA was repressed by p53 siRNA by 63% relative to that of control ( P < 0.05; Fig. 1 B ). Fig. 1. p53 represses Lasp1 transcription.
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 …
WebMar 24, 2004 · The p53 gene was inactivated in HCT116 p53 −/− cells by homologous recombination. Briefly, two promoterless targeting vectors containing either a geneticin or hygromycin resistance gene in place of genomic p53 sequences were sequentially transfected into HCT116 p53 +/+ cells to disrupt both p53 alleles (12). 名古屋 青柳 かえるまんじゅうWebApr 13, 2024 · HCT116 p53 −/− cells were cultured in a DMEM medium (Lonza) supplemented with 10% FBS, 100 U/mL of penicillin-streptomycin, 1 mM of sodium pyruvate, and 1× MEM non-essential amino acid (Sigma-Aldrich). All cells were incubated in a humidified incubator (95% air, 5% CO 2) at 37 °C. 2.3. Drugs and Compounds 名古屋駅 お土産売り場 キーホルダーWebDec 2, 2005 · p53 is the most frequently mutated gene in human cancer (Greenblatt et al, 1994). It exerts tumour-suppressor activity, regulating the cell cycle, programmed cell death and DNA repair. p53 functions are mediated by mechanisms that are transcriptional (Yu et al, 1999) and non-transcriptional (Mihara et al, 2003) dependent. 名古屋 青森 格安 パックWebFigure 1 Exposure of four Hct116 cell lines with (+) and without (-) Chk2 and p53 genes to 1 µM C5M So we can see that the Chk2+ means that it has that gene, and the Chk2- means that we knocked out the gene. There’s not really a difference between those two. And the reason we know that is by looking at the error bars. 名古屋駅 カフェ ゆっくりできるWebMar 24, 2024 · PGA 2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells. In contrast to apoptosis in HCT116 cells, PGA may induce apoptosis in a fashion of less potency, which is independent of p53 and DNA-PK in HCT116 p53-/- cells. 名古屋駅 エスカ 出口WebTo demonstrate that the p53-Luc fusion retains p53 function, we utilized HCT116 p53–/– cells (kindly provided by Dr B. Vogelstein). The pZ p53-Luc expression plasmid was stably transfected into HCT116 p53–/– cells and the resulting clones were used for … 名古屋 飲食店 おすすめWebMay 21, 2024 · These included HCT116, HCT116.p53 mutant, RKO, and RKO.p53 -/- lines (all from colon cancers) as well as breast cancer cell lines MCF7 and 1001 (MCF7-p53 mutant clone). HeLa cell line was used as a positive control for epithelial to mesenchymal transition (EMT). 名古屋 青い ケーキ