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LncEPAT-induced by EGFR inhibits USP16-mediated H2A deubiquitination

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE207441 | GEO | 2022/08/16

REPOSITORIES: GEO

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USP16-mediated Histone H2A Lysine-119 Deubiquitination during Oocyte Maturation is a Prerequisite for Zygotic Genome Activation

Project description:Maternal-to-zygotic transition (MZT) is the first and key step in the control of animal development and is intimately related to changes of chromatin structure and histone modifications. Mono-ubiquitination of histone H2A at lysine-119 (H2AK119ub1), an important epigenetic modification in regulating chromatin configuration and function, is primarily catalyzed by polycomb repressive complex 1 (PRC1) and contributes to resistance to transcriptional reprogramming in mouse embryos. In this study, the genome-wide dynamic distribution of H2AK119ub1 during MZT in mice was investigated by chromosome immunoprecipitation and sequencing. The results indicated that H2AK119ub1 accumulated in fully grown oocytes, enriched at the transcriptional start sequences (TSSs) of maternal genes, but was promptly removed after meiotic resumption, particularly at the TSSs of early zygotic genes, by a previously unidentified mechanism. Genetic evidences indicated that ubiquitin-specific peptidase 16 (USP16) is the major deubiquitinase of H2AK119ub1 in mouse oocytes. Conditional knockout of Usp16 in oocytes did not impair their survival, growth, andor meiotic maturation. However, oocytes lacking USP16 were unable to undergo zygotic genome activation or gain developmental competence after fertilization, due to high levels of H2AK119ub1 deposition on the zygotic genomes. Taken together, this study indicates that H2AK119ub1 is erased during oocyte maturation by an USP16-dependent mechanism, which ensures zygotic genome reprogramming and transcriptional activation of essential early zygotic genes.

2022-06-05 | GSE154412 | GEO

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

2014-05-02 | E-GEOD-52899 | biostudies-arrayexpress

Usp16 deletion-induced gene expression in MEFs

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

2021-07-20 | GSE160485 | GEO

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)

2014-05-02 | GSE52899 | GEO

USP16 knockdown-induced gene expression in NCI-H23 cells

Project description:To determine the molecular signaling pathways responsible for USP16 regulation of cell growth, RNA sequencing was conducted on NCI-H23 cells with or without USP16 knockdown

2021-07-20 | GSE160388 | GEO

Analysis of gene expression in USP16 knockdown PC3 prostate cancer cells

Project description:Total RNA was obtained from PC3 cells with or without USP16 knockdown to perform a High-throughput sequencing. In our study, USP16 is necessary for prostate cancer cell proliferation in vitro and in vivo. Therefore, we perform the RNA-seq to explore potential mechanisms of USP16 regulating cell growth.

2023-11-01 | GSE160818 | GEO

Usp16 ChIP-seq of ckit and sca1 positive cells

Project description:anti-Usp16 ChIP-seq in ckit and sca1 hematopoietic stem/progenitor cells

2015-12-30 | GSE62823 | GEO

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

Project description:RNA-seq in wt and Usp16 deleted HSC/P

2015-12-30 | GSE62824 | GEO

AP-MS analysis of human RIOK1 and USP16

Project description:To discover novel factors involved in the final steps of 40S ribosomal subunit biogenesis in human cells, we isolated late cytoplasmic 40S subunit precursors by affinity purification (AP) of the assembly factor RIOK1. Subsequent analysis of their composition by mass spectrometry (MS) led to identification of the deubiquitinase USP16. AP-MS of USP16 confirms that it is a component of late cytoplasmic pre-40S particles and we further show that USP16 possesses a new, ribosome-associated function.

2020-03-04 | PXD016458 | Pride

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.

2023-09-05 | GSE242032 | GEO

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