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Usp16 deletion-induced gene expression in MEFs

ABSTRACT: To determine the molecular signaling pathways responsible for USP16 regulation of cell growth, RNA sequencing was conducted on MEFs with or without Usp16 deletion

ORGANISM(S): Mus musculus

PROVIDER: GSE160485 | GEO | 2021/07/20

REPOSITORIES: GEO

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Usp16 deletion-induced gene expression in MEFs

Project description:Usp16 deletion-induced gene expression in MEFs

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Genome-wide maps of Usp16, ubH2A and gene expression profiles in wild type and Usp16 knock out mouse embryonic stem cells (ESCs) and embryoid bodies (EBs)

Project description:Polycomb Repressive Complex 1 and histone H2A ubiquitination (ubH2A) contribute to embryonic stem cell (ESC) pluripotency by repressing lineage-specific gene expression. However, whether active deubiquitination co-regulates ubH2A levels in ESCs and during differentiation is not known. Here, we report that the histone H2A deubiquitinase Usp16 regulates H2A deubiquitination and gene expression in ESCs, and importantly, is required for ESC differentiation. Usp16 knockout is embryonic lethal in mice, but does not affect ESC viability or identity. Usp16 binds to the promoter regions of a large number of genes in ESCs and Usp16 binding is inversely correlated with ubH2A levels and positively correlated with gene expression levels. Intriguingly, Usp16-/- ESCs fail to differentiate due to ubH2A-mediated repression of lineage-specific genes. Finally, Usp16, but not the enzymatically inactive mutant, rescues the differentiation defects of Usp16-/- ESCs. Therefore, this study identifies Usp16 and H2A deubiquitination as critical regulators of ESC gene expression and differentiation. Examination of binding pattern of H2A deubiquitinase Usp16 and ubH2A in mouse embryonic stem cells and embroid bodies

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LncEPAT-induced by EGFR inhibits USP16-mediated H2A deubiquitination

Project description:Depleting lncEPAT in GBM cells leads to altered cell-senescence related gene expression, and this phenotype can be reversed by USP16 further knock-down.

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Genome-wide maps of Usp16, ubH2A and gene expression profiles in wild type and Usp16 knock out mouse embryonic stem cells (ESCs) and embryoid bodies (EBs)

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FGF18 alleviates hepatic ischemia-reperfusion injury via the USP16-mediated KEAP1/Nrf2 signaling pathway in male mice

Project description:Hepatic ischemia-reperfusion injury (IRI) is a common complication occurs during hepatic resection and transplantation. However, the mechanisms underlying hepatic IRI have not been fully elucidated. Here, we aim to explore the role of fibroblast growth factor 18 (FGF18) in hepatic IRI. In this work, we find that Hepatic stellate cells (HSCs) secrete FGF18 and alleviates hepatocytes injury. HSCs-specific FGF18 deletion largely aggravates hepatic IRI. Mechanistically, FGF18 treatment reduces the levels of ubiquitin carboxyl-terminal hydrolase 16 (USP16), leading to increased ubiquitination levels of Kelch Like ECH Associated Protein 1 (KEAP1) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, USP16 interacts and deubiquitinates KEAP1. More importantly, Nrf2 directly binds to the promoter of USP16 and forms a negative feedback loop with USP16. Collectively, our results show FGF18 alleviates hepatic IRI by USP16/KEAP1/Nrf2 signaling pathway in male mice, suggesting that FGF18 represents a promising therapeutic approach for hepatic IRI.

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Usp16 WT and KO RNA-Seq ckit and sca1 positive cells

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AP-MS analysis of human RIOK1 and USP16

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