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Effect of iASPP knockout in mouse keratinocytes

ABSTRACT: Effect of iASPP knockout in mouse keratinocytes

PROVIDER: PRJNA778802 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16848200.fastq.gz	Fastqsanger.gz
	SRR16848201.fastq.gz	Fastqsanger.gz
	SRR16848202.fastq.gz	Fastqsanger.gz
	SRR16848203.fastq.gz	Fastqsanger.gz
	SRR16873033_1.fastq.gz	Fastqsanger.gz

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Transcriptional impact of iASPP knockout in mouse keratinocytes

Project description:iASPP (PPP1R13L) is an evolutionarily conserved regulator of p53 family members. In mice, iASPP deletion in keratin 14-expressing keratinocytes is sufficient to cause detrimental phenotypes with squamous epithelium abnormalities. In human skin, wild-type nuclear iASPP colocalizes with the key squamous differentiation regulatory factor, TP63, and iASPP mutations also show abnormalities in skin development. To clarify how iASPP influences the keratinocyte transcriptome, iASPP WT and iASPP KO primary mouse keratinocytes (MKC) were compared.

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Transcriptional impact of iASPP knockout in mouse keratinocytes

Project description:Transcriptional impact of iASPP knockout in mouse keratinocytes

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Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

Project description:iASPP (PPP1R13L) is an evolutionarily conserved regulator of p53 family members. In mice, iASPP deletion in keratin 14-expressing keratinocytes is sufficient to cause detrimental phenotypes with squamous epithelium abnormalities. In human skin, wild-type nuclear iASPP colocalizes with the key squamous differentiation regulatory factor, TP63, and iASPP mutations are associated with abnormalities in skin development. To clarify how iASPP modulates p63 genome occupancy, p63 ChIP-seq data from iASPP WT and iASPP KO primary mouse keratinocytes (MKC) were compared.

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Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

Project description:Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

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Effect of iASPP knockout in mouse keratinocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effect of FAM50 knockout on the transcriptome

Project description:A knockout clone has been generated for both FAM50A and FAM50B; knockout of the other gene is then performed and the transcriptome is analysed to look at the effect of dual gene loss.

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Selective and direct p53 inhibition by iASPP

Project description:We performed p53 ChIP-seq analysis of Nutlin-treated HCT116 cells to identify high-confident p53 regulated targets. And we performed ChIP-seq using an anti-p53 antibody in HCT116 cells treated with control or iASPP RNAi to identify iASPP regulated p53 targets.

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Project description:Maintenance of immunological homeostasis between tolerance and autoimmunity is essential for the prevention of human diseases ranging from autoimmune disease to cancer. Accumulating evidence suggests that p53 can mitigate phagocytosis-induced adjuvanticity thereby promoting immunological tolerance following programmed cell death. Here we identify Inhibitor of Apoptosis Stimulating p53 Protein (iASPP), a negative regulator of p53 transcriptional activity, as a regulator of immunological tolerance. iASPP-deficiency promoted lung adenocarcinoma and pancreatic cancer tumorigenesis, while iASPP-deficient mice were less susceptible to autoimmune disease. Immune responses to iASPP-deficient tumors exhibited hallmarks of immunosuppression, including activated regulatory T cells and exhausted CD8+ T cells. Interestingly, iASPP-deficient tumor cells and tumor-infiltrating myeloid cells, CD4+, and gd T cells expressed elevated levels of PD-1H, a recently identified transcriptional target of p53 that promotes tolerogenic phagocytosis. Identification of an iASPP/p53 axis of immune homeostasis provides a therapeutic opportunity for both autoimmune disease and cancer.

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Regulation of Immunological Tolerance by the p53-Inhibitor iASPP

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Regulation of Immunological Tolerance by the p53-Inhibitor iASPP [mNET-Seq]

Project description:Maintenance of immunological homeostasis between tolerance and autoimmunity is essential for the prevention of human diseases ranging from autoimmune disease to cancer. Accumulating evidence suggests that p53 can mitigate phagocytosis-induced adjuvanticity thereby promoting immunological tolerance following programmed cell death. Here we identify Inhibitor of Apoptosis Stimulating p53 Protein (iASPP), a negative regulator of p53 transcriptional activity, as a regulator of immunological tolerance. iASPP-deficiency promoted lung adenocarcinoma and pancreatic cancer tumorigenesis, while iASPP-deficient mice were less susceptible to autoimmune disease. Immune responses to iASPP-deficient tumors exhibited hallmarks of immunosuppression, including activated regulatory T cells and exhausted CD8+ T cells. Interestingly, iASPP-deficient tumor cells and tumor-infiltrating myeloid cells, CD4+, and gamma-delta T cells expressed elevated levels of PD-1H, a recently identified transcriptional target of p53 that promotes tolerogenic phagocytosis. Identification of an iASPP/p53 axis of immune homeostasis provides a therapeutic opportunity for both autoimmune disease and cancer.

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