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Differentially expressed genes in Gdown1 knockout and Gdown1/p53 double-knockout mouse liver [RNA-seq]

ABSTRACT: Differentially expressed genes in Gdown1 knockout and Gdown1/p53 double-knockout mouse liver [RNA-seq]

PROVIDER: PRJNA603066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10961169.fastq.gz	Fastqsanger.gz
	SRR10961170.fastq.gz	Fastqsanger.gz
	SRR10961171.fastq.gz	Fastqsanger.gz
	SRR10961172.fastq.gz	Fastqsanger.gz
	SRR10961173.fastq.gz	Fastqsanger.gz

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Differentially expressed genes in Gdown1 knockout and Gdown1/p53 double-knockout mouse liver [RNA-seq]

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p53 binding during the DNA double-strand break response

Project description:We used ChIP-seq to assess where p53 binds in the human genome and how that binding changes during the DNA double-strand break response. In particular, we considered the 1-Mb-wide window centered on the MYC locus. Contrary to previous reports, we found no evidence of p53 binding at the MYC promoter. Rather, we identified three locations downstream of MYC at which p53 was bound; binding at each of these regions increased during the DNA double-strand break response.

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Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

Project description:Purpose: Citron kinase (CitK) knockout mice show a severe form of primary microcephaly, associated with ataxia and lethal epilepsy. This phenotype is caused by massive apoptosis occuring during embryonic and post-natal brain development, associated with cytokinesis failure. Cerebellum is the tissue showing highest sensitivity to CitK loss. The clinical phenotype of CitK knockout mice is significantly resued by P53 inactivation. In addition, CitK/P53 double knockout brains have almost normal levels of apoptosis, but display high percentage of binucleated and multinucleated cells. The aim of this study was to analyze the gene expression changes produced in developing neural tissue by CitK loss and to determine which alterations are P53-dependent. expression changes Methods: We analyzed by RNA sequencing total RNA extracted from P4 cerebellum of mice characterized by the following genotypes: 1. CitK +/-, P53 +/- (CTRL); 2. CitK -/-, P53 +/- (CitK-KO); 3. CitK +/-, P53 -/- (P53-KO); 4. CitK -/-, P53 -/- (D-KO). Biological triplicates were analyzed per every genotype. Conclusions: The loss of CitK leads to a strong reduction of the expression of pro-neural genes and induces a P53-related pro-apoptotic gene sets. The analysis of D-KO mice reveals that most of these changes are P53-dependent, but many genes implicated in growth arrest are induced through P53-independent mechanisms.

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Expression data of dorsolateral prostates from wild type, prostate-specific Pten knockout, and prostate-specific Pten and Pml double knockout mice

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