Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HyperTRIBE assay of VSV-GFP-infected HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein

ABSTRACT: To explore the binding sites of PTENα on viral or host RNAs, we performed HyperTRIBE assay of HEK293T cells overexpressing ADAR1-CD, PTENα-N(WT)-ADAR1-CD, or PTENα-N(6R/D)-ADAR1-CD fusion protein under VSV-GFP (green fluorescent protein-expressing vesicular stomatitis virus) infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237910 | GEO | 2024/02/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of wild-type and Ptenα-/- MEFs under VSV infection

Project description:To explore the effect of Ptenα on antiviral immunity pathway, we conducted RNA transcriptome profiling of wild-type and Ptenα-/- MEFs (mouse embryonic fibroblast cells) in response to VSV (vesicular stomatitis virus)

2024-02-19 | GSE210684 | GEO

UV cross-linking RIP-seq of VSV-GFP-infected HEK293T cells overexpressed PTENα

Project description:To determine whether PTENα directly binds to viral RNA or host mRNA, we performed UV cross-linking RNA immunoprecipitation (RIP) sequencing of HEK293T cells transfected with vector encoding PTENα under VSV-GFP (green fluorescent protein-expressing vesicular stomatitis virus) infection

2024-02-19 | GSE218439 | GEO

The role of PTENα in brain

Project description:In contrast to the ubiquitous expression profile of PTEN, PTENα is predominantly expressed in brain. To study the biological function of PTENα in brain, we employed LCMV to induce murine viral encephalitis model. Through single cell RNA sequencing, we revealed the immunological function of PTENα during viral infection in the brain.

2023-07-31 | GSE238151 | GEO

Mechanistic Implications of Enhanced Editing by a HyperTRIBE RNA-binding protein

Project description:Most current methods to identify cell-specific RNA binding protein (RBP) targets require analyzing an extract, a strategy that is problematic with small amounts of material. We previously addressed this issue by developing TRIBE, a method that expresses an RBP of interest fused to the catalytic domain (cd) of the RNA editing enzyme ADAR. TRIBE performs Adenosine-to-Inosine editing on candidate RNA targets of the RBP. However, target identification is limited by the efficiency of the ADARcd. Here we describe HyperTRIBE, which carries a previously characterized hyperactive mutation (E488Q) of the ADARcd. HyperTRIBE identifies dramatically more editing sites than TRIBE, many of which are also edited by TRIBE but at a much lower editing frequency. The data have mechanistic implications for the enhanced editing activity of the HyperADARcd as part of a RBP fusion protein and also indicate that HyperTRIBE more faithfully recapitulates the known binding specificity of its RBP than TRIBE.

2017-08-19 | GSE102814 | GEO

scRNA-seq analysis of tumor infiltrating lymphocytes in PTENα-expressing tumors

Project description:As a tumor suppressor, PTEN is frequently mutated in human cancers and PTEN mutants promote tumor progression and metastasis. PTEN mutations have been implicated in immune regulation, but the underlying mechanism is largely unknown. We report that PTENα, the isoform of PTEN, remains active in cancer bearing stop-gained PTEN mutations. Through counteraction of CD8+ T cell-mediated cytotoxicity, presence of PTENα leads to T cell dysfunction and accelerates immune-resistant cancer progression. Clinical analysis further uncovers that PTENα-active mutations suppress host immune responses and result in poor prognosis in cancer as relative to PTENα-inactive mutations. Furthermore, germline deletion of Ptenα in mice increases cell susceptibility to immune attack through augmenting stress granule formation and limiting synthesis of peroxidases, leading to massive oxidative cell death and severe inflammatory damage. We propose that PTENα protects tumor from T cell killing and thus PTENα is a potential target in antitumor immunotherapy.

2021-07-12 | GSE178258 | GEO

PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [RNA-seq]

Project description:we report that USP9X and FBXW11 selectively regulate the stability of PTENα/β but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTENα/β. In contrast to the current paradigm for PTEN as a tumor suppressor, PTENα/β promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTENα/β localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTENα/β but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature.

2019-02-26 | GSE126983 | GEO

PTENα/β paradoxically promote carcinogenesis through WDR5-H3K4me3 axis [ChIP-seq]

2019-02-26 | GSE126982 | GEO

PTENα functions as an immune suppressor and promotes immune resistance in PTEN-mutant cancer

2024-02-19 | GSE167469 | GEO

ADAR1 regulates melanoma progression via miRNAs biogenesis

Project description:Aberrant RNA-editing was observed in several human tumors, but its significance is mostly unknown. Here we show that ADAR1, a ubiquitous RNA-editing enzyme, is commonly lost in metastatic melanoma cells and specimens. Experimental ADAR1 silencing significantly alters melanoma cell morphology, facilitates proliferation and cell-cycle, and increases the tumorigenicity in-vivo. A series of ADAR1 truncation mutants establishes a novel RNA-editing-independent role for ADAR1 in controlling the nuclear and cytoplasmic processing steps of miRNA biogenesis. Altered expression of ADAR1-controled miRNAs accounts for the observed phenotype. We show that the oncogenic miR-17-5p endogenously regulates ADAR1 expression and that its genomic sequence is frequently amplified in melanoma to overexpress the mature miR-17-5p form. ADAR1 and miR-17-5p are ubiquitously expressed, suggesting the generality of this mechanism. Melanoma cell line expressing low ADAR1 levels (ADAR1-Knockdown) using shRNA technique were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to examine the alterations in the genes and microRNA expression profile in the manipulated cell system, due to ADAR1 possible involvement cancer development. To that end, we selected ADAR1-knockdown (ADAR1-KD) cells that demonstrated an enhanced aggressive phenotype both in vivo and in vitro as compared to the control cells (Control).

2012-08-31 | E-GEOD-31963 | biostudies-arrayexpress

ADAR1-editing in HeLa, p150-KO and ADAR1-KO transcriptomes

Project description:RNAseq analysis of cell lines with ADAR1-p150 and ADAR1-p110 knock-outs and primary human tissue samples (from GSE57353 and GSE99392 data sets) to identify sites of ADAR1 editing

2018-12-04 | GSE115127 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data