Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1137903 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29891559_1.fastq.gz | Fastqsanger.gz | |||
| SRR29891559_2.fastq.gz | Fastqsanger.gz | |||
| SRR29891560_1.fastq.gz | Fastqsanger.gz | |||
| SRR29891560_2.fastq.gz | Fastqsanger.gz | |||
| SRR29891561_1.fastq.gz | Fastqsanger.gz |
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Project description:Investigating the interaction of NUP153 to TBEV viral RNA
| PRJEB77840 | ENA
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.
2025-09-20 | GSE276333 | GEO
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
2015-06-19 | E-GEOD-64008 | biostudies-arrayexpress
Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) ORF57 is a viral RNA-binding protein essential for viral lytic gene expression. ORF57 binds to target RNA directly via interaction with cellular cofactors. To investigate the entire repertoire of ORF57-associated RNAs we performed UV cross-linking immunoprecipitatin (CLIP) experiment using an affinity-purified, highly specific anti-ORF57 antibody in KSHV-infected primariy effusion lymphoma BCBL-1 cells undegoing lytic virus replication.
2021-11-08 | GSE179726 | GEO
Project description:The identification of RNAs that are recognized by RNA-binding proteins (RNA-BPs) using techniques such as Crosslinking and Immunoprecipitation (CLIP) has revolutionized the genome-wide discovery of RNA-BP RNA targets. Among the different versions of CLIP that have been developed, the use of photoactivable nucleoside analogs has resulted in high efficiency photoactivable ribonucleoside-enhanced CLIP (PAR-CLIP) in vivo. Nonetheless, PAR-CLIP has not yet been applied in prokaryotes. To determine if PAR-CLIP can be used in prokaryotes, we determined suitable conditions for the incorporation of 4-thiouridine (4SU), a photoactivable nucleoside, into E. coli RNA and for the isolation of RNA crosslinked to RNA-BPs of interest. Applying this technique to Hfq, a well-characterized regulator of small RNA (sRNA)-messenger RNA (mRNA) interactions, we showed that PAR-CLIP identified most of the known sRNA targets of Hfq, as well as functionally relevant sites of Hfq-mRNA interactions at nucleotide resolution. Based on our findings, PAR-CLIP represents an improved method to identify both the RNAs and the specific regulatory sites that are recognized by RNA-BPs in prokaryotes.
2022-10-18 | MSV000090547 | MassIVE
Project description:Flavivirus infection involves extensive remodeling of the endoplasmic reticulum (ER), which is key to both the replication of the viral RNA genome as well as the assembly and release of new virions. Yet, little is known about how viral proteins and host factors cooperatively facilitate such a vast transformation of the ER, and how this influences the different steps of the viral life cycle. In this study, we screened for host proteins that interact with the tick-borne encephalitis virus (TBEV) protein NS4B and found that the top candidates were coupled to trafficking between ER exit sites (ERES) and the Golgi. We characterized the role of ACBD3, one of the identified proteins, in flavivirus infection and show that it interacts with NS4B to promote infection across multiple flavivirus species. Using ACBD3 knockout cells, we found that the depletion of ACBD3 inhibited TBEV replication by preventing the trafficking of virions from the cell. We found that ACBD3 promotes flavivirus infection via a different mechanism than its previously described role in picornavirus infection. ACBD3 was enriched at modified ERES-Golgi contact sites to support virus replication. Therefore, we propose that ACBD3 promotes flavivirus replication by modifying the trafficking between the ERES and the Golgi to enable the release of new virions.
2025-03-31 | PXD051173 | Pride
Project description:Bulk RNA-seq comparison of neurons, astrocytes and microglia, after infection with LGTV, TBEV and control.
2023-10-27 | E-MTAB-12902 | biostudies-arrayexpress
Project description:Master transcription factors such as TP63 establish super-enhancers (SEs) to drive core transcriptional networks in cancer cells, yet the spatiotemporal regulation of SEs within the nucleus remains unknown. The nuclear pore complex (NPC) may tether SEs to the nuclear pore where RNA export rates are maximal. Here, we report that NUP153, a component of the NPC, anchors SEs to the NPC and enhances TP63 expression by maximizing mRNA export. This anchoring is mediated through protein-protein interaction between the intrinsically disordered regions (IDRs) of NUP153 and the coactivator BRD4. Silencing of NUP153 excludes SEs from the nuclear periphery, decreases TP63 expression, impairs cellular growth, and induces epidermal differentiation of squamous cell carcinoma. Overall, this work reveals the critical roles of NUP153 IDRs in the regulation of SE localization, thus providing insights into a new layer of gene regulation at the epigenomic and spatial level.
2023-12-23 | GSE169295 | GEO
Project description:Alphaviruses are arthropod-borne viruses that represent a significant threat to public health at a global level. While the formation of alphaviral nucleocapsid cores, consisting of cargo nucleic acid and the viral capsid protein, is an essential molecular process of infection, the precise interactions between the two partners are ill-defined. A CLIP-seq approach was used to screen for candidate sites of interaction between the viral Capsid protein and genomic RNA of Sindbis virus (SINV), a model alphavirus. The data presented in this report indicates that the SINV capsid protein binds to specific viral RNA sequences in the cytoplasm of infected cells, but its interaction with genomic RNA in mature extracellular viral particles is largely non-specific in terms of nucleotide sequence. Mutational analyses of the cytoplasmic viral RNA-capsid interaction sites revealed a functional role for capsid binding early in infection. Interaction site mutants exhibited decreased viral growth kinetics; however, this defect was not a function of decreased particle production. Rather mutation of the cytoplasmic capsid-RNA interaction sites negatively affected the functional capacity of the incoming viral genomic RNAs leading to decreased infectivity. Furthermore, cytoplasmic capsid interaction site mutants are attenuated in a murine model of neurotropic alphavirus infection. Collectively, the findings of this study indicate that the identified cytoplasmic interactions of the viral capsid protein and genomic RNA, while not essential for particle formation, are necessary for genomic RNA function early during infection. This previously unappreciated role of capsid protein during the alphaviral replication cycle also constitutes a novel virulence determinant.
2017-06-19 | GSE99879 | GEO