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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

ABSTRACT: Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

PROVIDER: PRJNA779981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16931919_1.fastq.gz	Fastqsanger.gz
	SRR16931919_2.fastq.gz	Fastqsanger.gz
	SRR16931920_1.fastq.gz	Fastqsanger.gz
	SRR16931920_2.fastq.gz	Fastqsanger.gz
	SRR16931921_1.fastq.gz	Fastqsanger.gz

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:The goal of this study is to compare the sex specific effects of the expression of p53 missense mutations on the transcriptomes of male and female primary astrocytes. Primary cortical astrocytes harboring a single floxed Trp53 allele were harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. mRNA was collected from male and female astrocytes transduce with mouse Trp53:R172H, Trp53:Y202C, or Trp53:Y217C. This study revealed sex specific gain-of-function effects on the transcriptomes of each cell line that correlated with cancer pathways.

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis

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Project description:We have identified a relatively rare mutation in p53 in an Indian oral cancer patient sample at the fade end of its DNA binding domain [P152L]. Although P152L p53 DBD potentially binds to DNA, the full length protein is completely devoid of cognate site DNA binding ability. Also the mutant protein can efficiently tetramerize. Significantly, this mutant was found to induce cell mobility and proliferation with greater tumorigenic potential in nude mice, the mechanistic details of which is also investigated upon. These data establish P152L as a new gain of function p53 mutation

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Prevalent p53 gain-of-function mutants co-opt epigenetic pathways to drive cancer growth

Project description:We investigated the genomewide binding pattern of prevalent p53 gain-of-function (GOF) mutants by ChIP-seq, in a panel of breast cancer cell lines. We assessed the genomewide changes of H3K4me3 upon GOF p53 knockdown in MDA-MB-468 breast cancer cells bearing the p53 R273H mutation. This study uses ChIP-seq of H3K4me3 and histone H3 in wild-type or p53 R172H knock-in MEFs. Additionally, this study examines the transcriptome of wild-type or p53 R172H knock-in MEFs using polyA+ RNA-seq.

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