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Association of NUP153 on genomic DNA in TE5 cells [ChIP-seq]

ABSTRACT: Association of NUP153 on genomic DNA in TE5 cells [ChIP-seq]

PROVIDER: PRJNA826342 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18740847.fastq.gz	Fastqsanger.gz

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Association of NUP153 on genomic DNA in TE5 cells [ChIP-seq]

Project description:To understand the regulatory regions of genomic DNA by nuclear pore, the genomic region associated by NUP153, one of nuclear pore protein, was determined by Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) .

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ChiP-chip profiling of Drosophila melanogaster cell lines to identify targets for nuclear pore proteins Nup153 and Megator.

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Novel function of NUP153 in HNF4α transcriptional upregulation contributes to promoting HBV replication

Project description:Background & Aims: Nucleoporin 153 (NUP153) is known to facilitate the nuclear entry of the human immunodeficiency virus (HIV) nucleocapsid. Studies had also showed that immature hepatitis B virus (HBV) nucleocapsids can be arrested by NUP153, allowing them to further mature. In this study, we investigated the impact and specific mechanisms of NUP153 on HBV replication. Methods: NUP153 was knocked down using RNA interference or over-expressed through an expression plasmid in HBV cell models or in vivo in HBV-replicating mice. Luciferase reporter assays were employed to assess the activities of viral or host factor promoters. Cytoplasmic and nuclear fractionation experiments were conducted to analyze the subcellular distribution of proteins and HBV RNA. Results: In the present study, we found that HBV induced significant upregulation of NUP153 mRNA and protein in HBV cell models and HBV infected patients. Overexpression of NUP153 would markedly increase covalently closed circular DNA (cccDNA) transcription activity and progeny virus production, while downregulation of NUP153 could significantly inhibit HBV replication without affecting HBV cccDNA level directly. Similar results were observed in mice model hydrodynamically injected (HDI) with 1.2×HBV plasmid. HBV promoter assays revealed that NUP153 could promote HBV core promoter activity, likely in a hepatocyte nuclear factor 4α (HNF4α) dependent manner. Mechanistically, ERK signaling was required for NUP153-mediated promotion of HNF4α and HBV replication. Conclusions: The study here suggested that host factor NUP153 which reciprocally upregulated by the virus, is an important positive regulator of HBV replication. It also suggested that the NUP153-HBV positive feedback loop could serve as a potential therapeutic target.

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Nucleoporin Nup153 Regulates Stem Cell Pluripotency through Gene Silencing

Project description:Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), the transport channels that mediate nuclear transport. Recent evidence suggest that several Nups have additional roles in controlling the activation and silencing of developmental genes, however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the de-repression of developmental genes and induction of early differentiation. This loss of pluripotency is not associated with defects in global nucleo-cytoplasmic transport activity. Instead, Nup153 binds to the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb repressive complex 1 (PRC1) to its target loci. Our results reveal a nuclear transport-independent role of Nup153 in maintaining stem cell pluripotency and introduce a role of NPC proteins in mammalian epigenetic gene silencing. RNA-seq, ChIP-Seq, and DamID-Seq for Nup153, Oct4, and key chromatin regulators in mouse ES cells and neural progenitors

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Nucleoporin Nup153 Regulates Stem Cell Pluripotency through Gene Silencing

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