Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of RNA-binding protein interactors of duck lncrna (lnc455) using Multiple Oligo-assisted RNA Pulldown with Hybridization followed by Mass Spectrometry (MORPH-MS)

ABSTRACT: This project used MORPH-MS to identify proteins that interact with a duck lncRNA called lnc455, which is linked to antiviral responses. While lnc455 was predicted to enhance RIG-I/MAVS signaling, its effects appeared to be indirect. Using MORPH-MS, we mapped the lncRNA’s binding partners and uncovered several proteins known to suppress interferon signaling. This highlights how lnc455 may support antiviral immunity by blocking these negative regulators. The study also shows how MORPH-MS can uncover RNA–protein interactions in non-model species like ducks.

INSTRUMENT(S):

ORGANISM(S): Gallus Gallus (chicken)

TISSUE(S): Fibroblast

SUBMITTER: Renald James Legaspi

LAB HEAD: Katharine Edens Magor

PROVIDER: PXD067094 | Pride | 2026-04-27

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	checksum.txt	Txt
	morph-ms-lnc455-rep1-control.mgf	Mgf
	morph-ms-lnc455-rep1-control.mzTab	Mztab
	morph-ms-lnc455-rep1-control.raw	Raw
	morph-ms-lnc455-rep1-ubp.mgf	Mgf

Items per page:

1 - 5 of 19

Publications

Duck lncRNA lnc455 enhances RIG-I/MAVS type I interferon signaling by modulating hnRNPAB-mediated regulation of MAVS signaling.

Legaspi Renald James RJ Magor Katharine E KE

Scientific reports 20260310 1

Long non-coding RNAs (lncRNAs) regulate antiviral immunity against influenza A viruses, yet their roles in natural reservoir hosts like ducks remain unclear. In ducks, Retinoic acid-inducible gene I (RIG-I) contributes to their resistance to infection. To identify duck lncRNAs involved in RIG-I-mediated antiviral responses, we analyzed transcriptomic data from highly pathogenic avian influenza (HPAI)-infected duck lung tissues and identified lnc455 co-expressed with IFNβ. In-silico predictions s ...[more]

PMID: 41807513

Similar Datasets

BANC-seq to identify genome-wide transcription factor binding affinities to native chromatin

Project description:BANC-seq (Binding Affinities to Native Chromatin by sequencing) allows determination of absolute apparent binding affinites of transcription factors to native chromatin in a genome-wide manner. In this study, we establish the method and show that chromatin and DNA sequence define binding affinites of FOXA1, SP1, YY1 and MYC/MAX complex. To relate the identified binding affinities to the actual transcriptional levels of these transcription factors in the cells used in this study, and to confirm that the nuclear isolation protocol used in the study does not lead to loss of nuclear proteins, we have generated whole proteomes including proteomics standards for absolute quantification of proteins. In addition, to validate some of the findings of the study, we have performed PAQMAN (Protein-nucleic acid affinity quantification by MAss spectrometry in nuclear extracts), as well as DNA pulldowns followed by mass spec.

2023-02-09 | PXD038502 | Pride

Dissecting genotype-specific effects of disease-associated genetic variants

Project description:Background For many complex diseases, including Parkinson’s disease, regulatory elements located in intergenic regions have been putatively associated with disease risk and development. However, the biological mechanisms linking these intergenic loci to disease pathogenesis remain largely unknown. Fundamentally, this is because these intergenic loci are non-coding, and bespoke approaches to in-depth functional characterisation are required. Here we utilised an integrative, functional approach to identify the genotype-specific impacts of Parkinson’s disease-associated variant rs11610045, located within a complex region on chromosome 12. Methods & Results We utilised CRISPR-Cas9 editing (and reversal) to generate isogenic iPSC clones from the KOLF2.1J line containing either the A|A (WT) or G|G (edited) rs11610045 genotype. We also reverted the G|G genotype back to the A|A genotype in two clones to control for off-target effects. Functional profiling of these clones demonstrated allele-specific regulation of both nearby and distal genes, including THBS1 and PDGFB. Further, affinity purification followed by mass spectrometry identified the differential binding of potential regulatory proteins to the G|G genotype compared to the WT A|A genotype, including the transcription factor TCF7L1. Conclusions Our findings support a model in which non-coding variants, such as rs11610045, impact the expression and downstream activity of multiple genes predominantly through trans-acting mechanisms. In so doing, this study demonstrates a pipeline to delineate SNP-specific impacts in an iPSC model. Finally, we highlight the challenge of aligning genotype dependent expectations of the impact of expression quantitative loci on genes as part of the exploration of how inherited genetic variation contributes to complex genetic disease.

2026-04-07 | PXD065108 | Pride

Mapping functional non-coding variation in individual human genomes through haplotyping, multiomics, and deep learning

Project description:Most genetic variants in the human genome reside in non-coding regions, where they can perturb regulatory elements, influence gene expression, and contribute to various phenotypes and diseases. However, identifying such functionally relevant genetic variation remains challenging. Here we integrate personal genomics, allele-specific gene regulation, and deep learning predictions to map the impact of non-coding variation in its native allelic and regulatory context. We identify and validate hundreds of cell-type-specific transcription factor binding events disrupted by genetic variants, providing mechanistic insights underlying allele-specific gene regulation. Using this framework, we discover a rare variant that modulates PIK3R5 gene expression by disrupting an OCT2 binding site within a distal enhancer. Our study establishes a generalisable strategy for interpreting non-coding regulatory variation, enabling systematic dissection of variant effects across diverse biological systems and offering an alternative framework to investigate the disease mechanisms.

2026-04-22 | PXD069116 | Pride

FXR controls gene expression independently of RXR at non-canonical response elements

Project description:The Farnesoid-X-Receptor (FXR) is a class II nuclear receptor (NR), a class that obligately heterodimerizes with the Retinoid-X-Receptor (RXR). FXR is expressed as 4 isoforms (α1-α4) activated by bile acids that drive transcription from response elements IR-1 (inverted repeat-1). We recently showed that FXR isoforms α2 and α4 bind to non-canonical response elements ER-2 (everted repeat-2), thereby increasing mitochondrial respiratory capacity and limiting de novo lipogenesis. Binding to ER-2 motifs in mouse liver organoids represented 89% of all FXR genome wide binding. However, mechanistic differences in FXR binding and activation from these two response elements remained unexplored. Using DNA pull down followed by mass-spectrometry, we show that RXR is not involved in FXR binding to ER-2 response elements. Instead, RXR inhibited FXR binding and activation from these elements in luciferase reporters. Genome wide, RXR-lacking FXR binding sites showed higher enrichment for ER-2 motifs in mouse liver. Pharmacological and mutational abrogation of FXR-RXR heterodimerization specifically retained ER-2 transactivation capacities in luciferase reporters and HepG2 cells. Transcriptome-wide, 25% of FXR targets were inhibited upon RXR overexpression, but specifically activated by a novel heterodimerization-deficient mutant FXRα2L434R. These genes were ER-2 responsive and were involved in lipid metabolism and ammonia detoxification. In conclusion, we discovered that RXR is not required and even inhibits binding of FXRα2 to ER-2. Thus, whereas FXR α1 and α3 seem to be genuine class II NR, FXRα2 and α4 are facultative class II at ER-2 motifs. This novel feature holds promise to exploit and tailor therapeutic responses to FXR agonism.

2024-11-12 | PXD047930 | Pride

Depletion of the RNA binding protein HNRNPD impairs homologous recombination by inhibiting DNA-end resection and inducing R-loop accumulation

Project description:DNA double strand break (DSB) repair through homologous recombination (HR) is crucial to maintain genome stability. DSB resection generates a single strand DNA intermediate, which is crucial for the HR process. We used a synthetic DNA structure, mimicking a resection intermediate, as a bait to identify proteins involved in this process. Among these, LC/MS analysis identified the RNA binding protein, HNRNPD. We found that HNRNPD was able to bind chromatin, although this binding occurred independently of DNA damage. However, upon damage, HNRNPD re-localized to γH2Ax foci and its silencing impaired CHK1 S345 phosphorylation and the DNA end resection process. Indeed, HNRNPD silencing reduced the ssDNA fraction upon camptothecin treatment and AsiSI-induced DSB resection and reduced RPA32 S4/8 phosphorylation. CRISPR/Cas9-mediated HNRNPD knockout impaired in vitro DNA resection and sensitized cells to camptothecin and olaparib treatment. We found that HNRNPD interacts with the heterogeneous nuclear ribonucleoprotein SAF-A previously associated with DNA damage repair. HNRNPD depletion resulted in an increased amount of RNA:DNA hybrids upon DNA damage . Both the expression of RNase H1 and RNA pol II inhibition recovered the ability to phosphorylate RPA32 S4/8 in HNRNPD knockout cells upon DNA damage, suggesting that RNA:DNA hybrid resolution likely rescues the defective DNA damage response of HNRNPD-depleted cells.

2019-02-26 | PXD012045 | Pride

SMiLE-seq sequencing data (illumina) of human transcription factors profiled in the Codebook/GRECO-BiT collaboration

Project description:We assayed 284 human transcription factors (TFs) for DNA binding using selective microfluidics-based ligand enrichment followed by sequencing (SMiLE-seq). These experiments were part of the Codebook/GRECO-BiT collaboration aiming to identify the DNA binding sites of yet-uncharacterized TFs. All data has already been demultiplexed and associated with the corresponding TFs.

2024-11-11 | E-MTAB-14598 | biostudies-arrayexpress

Quantitative proteomic analysis of proteins bound to rs452384-T or rs452384-C

Project description:This project focuses on the functional characterization of a risk variant (SNP) implicated in the predisposition to uveal melanoma, rs452384. We sought to determine whether some nuclear factors could bind with allele-specificity a DNA sequence centered around rs452384 to regulate gene expression. We sought to identify by quantitative mass spectrometry the nuclear proteins bound to double-stranded DNA probes with identical DNA sequences except for rs452384-C or T alleles in the center of the probe. The goal was to quantify the binding of transcription factors to the DNA probes, and to select those enriched (or specific) to the C or T allele of rs452384. To identify proteins specifically bound to rs452384, we compared binding partners to those obtained with a negative control probe known not to recognize any transcription factor.

2022-11-15 | PXD028954 | Pride

Lai_GM2/BS32/BS33

Project description:modENCODE_submission_3307 This submission comes from a modENCODE project of Eric Lai. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We plan to generate a comprehensive catalog of expressed and functional microRNAs, and generate biological evidence for their regulatory activity. We plan also to delineate the primary transcription units of microRNA genes. Finally, we plan to annotate other classes of non-miRNA expressed small RNAs, as least some of which may define novel classes of small RNA genes. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: RNA-seq. BIOLOGICAL SOURCE: Cell Line: GM2; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Unknown; EXPERIMENTAL FACTORS: Cell Line GM2

2010-10-18 | E-GEOD-24300 | biostudies-arrayexpress

Methylation-sensitive SMiLE-seq sequencing data (illumina) of human transcription factors profiled in the Codebook/GRECO-BiT collaboration

Project description:We assayed 114 human transcription factors (TFs) for DNA binding using methylation-sensitive selective microfluidics-based ligand enrichment followed by sequencing (meSMiLE-seq). Across 23 experiments, we identified DNA binding sites for 48 TFs. Among these, 13 showed aversion towards methylated DNA, while 11 exhibited either a preference for methylated DNA or an alternative binding site including the modification. The DNA binding for the remaining TFs was unaffected by DNA methylation under the conditions of the assay.

2024-11-11 | E-MTAB-14597 | biostudies-arrayexpress

RNA oligomers training set for the Pytheas scoring function

Project description:Mass spectrometry remains an important method for analysis of modified nucleosides ubiquitously present in cellular RNAs, in particular for ribosomal and transfer RNAs that play crucial roles in mRNA translation and decoding. Furthermore, modifications have effect on the lifetimes of nucleic acids in plasma and cells and are consequently incorporated into RNA therapeutics. To provide an analytical tool for sequence characterization of modified RNAs, we developed Pytheas, an open-source software package for automated analysis of tandem MS data for RNA. This dataset contains the 95 MS/MS spectra of 3-14 nts-long oligomers, used for the training and validation of Pytheas' scoring function.

2022-05-04 | PXD030435 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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