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Mus musculus

ABSTRACT: smallRNA-Seq analysis comparing p53-null versus ΔNp63Δ/Δ p53-null thymic lymphoma tumors

PROVIDER: PRJNA311955 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3167182.fastq.gz	Fastqsanger.gz
	SRR3167183.fastq.gz	Fastqsanger.gz
	SRR3167184.fastq.gz	Fastqsanger.gz
	SRR3167185.fastq.gz	Fastqsanger.gz
	SRR3167186.fastq.gz	Fastqsanger.gz

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smallRNA-Seq analysis comparing p53-null versus ΔNp63Δ/Δ;p53-null thymic lymphoma tumors

Project description:We performed a smallRNA-Seq analysis comparing thymic lymphoma tissues from the p53-null (n=4) and ΔNp63Δ/Δ;p53-/- (n=3). Mice at 10 weeks of age were injected with either Ad-mCherry or Ad-CRE-mCherry to delete ΔNp63 in the thymic lmyphomas. We aimed to test by deleting the ΔNp63 in these p53-deficient tumors will mediate tumor regression and analyze the expression profile of the small RNAs

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Project description:RNA-Seq analysis comparing p53-null versus ΔNp63Δ/Δ p53-null or ΔNp73Δ/Δ p53-null thymic lymphoma tumors

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RNA-Seq analysis comparing p53-null versus ΔNp63Δ/Δ;p53-null or ΔNp73Δ/Δ;p53-null thymic lymphoma tumors

Project description:We performed an RNA-Seq analysis comparing thymic lymphoma tissues from the p53-null(n=2) and ΔNp63Δ/Δ;p53-/- (n=3) or ΔNp73Δ/Δ;p53-/-(n=3). Mice at 10 weeks of age were injected with either Ad-mCherry or Ad-CRE-mCherry to delete ΔNp63/ΔNp73 in the thymic lmyphomas. We aimed to test by deleting the DNp63/DNp73 in these p53-deficient tumors will mediate tumor regression and analyze the expression profile of the genes Examination of thymic lymphoma tissues in 3 different genotypes (p53-/- vs ΔNp63Δ/Δ;p53-/- or ΔNp73Δ/Δ;p53-/-)

2014-11-19 | E-GEOD-60827 | biostudies-arrayexpress

RNA-Seq analysis comparing p53-null versus ΔNp63Δ/Δ;p53-null or ΔNp73Δ/Δ;p53-null thymic lymphoma tumors

2014-11-19 | GSE60827 | GEO

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Project description:ChIP-seq data of a thymic lymphoma cell line deriving from p53-null mice

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Unique Transcriptional Profiles Underlie Osteosarcomagenesis Driven by Different p53 Mutants (RNA-Seq)

Project description:To identify mutant p53 GOF, murine primary osteosarcomas expressing p53R172H or p53R245W over null and p53-null osteosarcomas were processed for bulk sequencing; DEGs were identified in p53R172H and p53R245W expressing tumors by comparing to p53-null tumors; DEGs were used to identify dysregulated pathways and mutant p53 GOF

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Project description:Gene expression profiling of P53/R26 +/+ (n=2) versus P53/R26-Zeb2tg/tg (n=3) thymic tumors

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RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

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LCK-mediated RIPK3 Activation Controls Double-Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A-ERK Axis

Project description:Receptor-interacting protein kinase 3 (RIPK3) is the primary regulator of necroptotic cell death. RIPK3 expression is often silenced in various cancer cells, which suggests that it may have tumor suppressor properties. However, the exact mechanism by which RIPK3 negatively regulates cancer development and progression remains unclear. This report indicates that RIPK3 acts as a potent regulator of homeostatic proliferation of CD4+CD8+ double-positive (DP) thymocytes. Abnormal proliferation of RIPK3-deficient DP thymocytes occurs independently of the well-known role for RIPK3 in necroptosis (upstream of MLKL activation), and is associated with an incidental thymic mass, likely thymic hyperplasia. In addition, Ripk3-null mice developed increased thymic tumor formation accompanied by reduced host survival in the context of a N-ethyl-N-nitrosourea (ENU)-induced tumor model. Moreover, RIPK3 deficiency in p53-null mice promoted thymic lymphoma development via upregulated ERK signaling, which correlated with markedly reduced survival rates. Mechanistically, lymphocyte-specific protein tyrosine kinase (LCK) activates RIPK3, which in turn leads to increases in the phosphatase activity of protein phosphatase 2 (PP2A), thereby suppressing hyper-activation of ERK in DP thymocytes. Overall, these findings suggest that a RIPK3-PP2A-ERK signaling axis regulates DP thymocyte homeostasis and may provide a potential therapeutic target to improve thymic lymphoma therapies.

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2019-10-18 | E-MTAB-8015 | biostudies-arrayexpress

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