RNAseq of mutant TP53 HCT116 cell line clones generated via CRISPR editing

·发布 2024年10月16日

114

样本数

114

实验数

实验描述

To compare the impact of several TP53 mutant variants in an isogenic setting, different TP53 mutations were introduced in HCT116 colorectal carcinoma cells. This parental cell line is wild-type for TP53 and shows a prototypical p53 response. To ensure unambigous genotype-phenotype correlations, the cell were haploidized prior to CRISPR-editing by introducing inactivating deletions of intronic splicing into one of the two TP53 alleles, leaving only one functional copy of TP53. The remaining TP53 allele was altered by inserting a LoxP-flanked transcriptional stop cassette (Lox-Stop-Lox, LSL) into intron 4, which allowed reversible silencing of TP53 expression. The LSL cassette was then specifically targeted with CRISPR/Cas9 to introduce a variety of different mutant p53 alleles. The competency of the mutated p53 allele to induce a p53 response upon activation using Nutlin-3a was then assessed in an RNAseq experiment.

样本属性

Organism

Homo sapiens

Developmental stage

adult

Disease

colorectal cancer

Organism part

colon

Cell line

HCT116

Genotype

TP53 Δ/C176F, TP53 Δ/R175X, TP53 Δ/G245S, TP53 Δ/V157F, TP53 Δ/R175H, TP53 Δ/Δ, TP53 Δ/LSL, TP53 Δ/R175P, TP53 Δ/WT, TP53 Δ/R248W, TP53 Δ/R248Q, TP53 Δ/R273H, TP53 Δ/Y220C, TP53 Δ/R249S, wild type genotype, ... 2 other values

实验信息

登记号

E-MTAB-12734

实验类型

RNA-seq of coding RNA

物种

Homo sapiens, Homo sapiens

发布日期

2024年10月16日

提交者

Marco Mernberger、 Julianne Funk、 Maria Klimovich、 Evangelos Pavlakis、 Michelle Neumann、 Daniel Drangenstein、 Maxim Noeparast、 Pascal Hunold、 Anna Borowek、 Dimitrios-Ilias Balourdas、 Katharina Kochhan、 Nastasja Merle、 Michael Wanzel、 Sabrina Elmshäuser、 Andrea Nist、 Marek Bartkuhn、 Katharina Humpert、 Rajkumar Savai、 Andreas Joerger、 Thorsten Stiewe

外部链接

ArrayExpress 原始页

分析服务

RNAseq of mutant TP53 HCT116 cell line clones generated via CRISPR editing

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