Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A defect in G-quadruplex binding disrupts AID chromatin localization

ABSTRACT: A defect in G-quadruplex binding disrupts AID chromatin localization

PROVIDER: PRJNA564109 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10074830_1.fastq.gz	Fastqsanger.gz
	SRR10074830_2.fastq.gz	Fastqsanger.gz
	SRR10074831_1.fastq.gz	Fastqsanger.gz
	SRR10074831_2.fastq.gz	Fastqsanger.gz
	SRR10074832_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

A defect in G-quadruplex binding disrupts AID chromatin localization

Project description:Activation-induced cytidine deaminase (AID) plays a vital role in adaptive immunity by enabling class switch recombination (CSR) and somatic hypermutation (SHM). While many molecular factors affect AID targeting and function, mounting evidence implicates G-quadruplex (G4) nucleic acid structures as critical effectors of AID biology. To examine the function of AID-G4 binding in vivo, we generated a knock-in mouse with a mutation in Aicda (AIDG133V) that disrupts AID-G4 binding without altering DNA deaminase activity. AIDG133V mice completely lack CSR and SHM, modeling the pathology of hyper-IgM syndrome patients with an orthologous mutation. ChIP-sequencing experiments reveal a broad defect in AIDG133V chromatin localization, implicating AID-G4 binding in genome-wide AID targeting. We find that major histocompatibility complex (MHC) class II genes are AID targets, and that increased AID expression in diffuse large B-cell lymphomas (DLBCLs) correlates with decreased MHC class II expression. Given that loss of MHC class II expression in DLBCLs is highly correlated with adverse outcomes, AID-dependent gene regulation may provide a novel therapeutic target.

2020-10-14 | GSE136959 | GEO

G-Quadruplex structures are stable and detectable in human genomic DNA.

Project description:The G-quadruplex is an alternative DNA structural motif that is considered to be functionally important in the mammalian genome. Herein, we address the hypothesis that G-quadruplex structures can exist within double-stranded genomic DNA using a G-quadruplex-specific probe. An engineered antibody is employed to enrich for DNA containing G-quadruplex structures, followed by deep sequencing to detect and map G-quadruplexes at high resolution in genomic DNA from human breast adenocarcinoma cells. Our high sensitivity structure-based pull-down strategy enables the isolation of genomic DNA fragments bearing a single as well as multiple G-quadruplex structures. Stable G-quadruplex structures are found in sub-telomeres, gene bodies and gene regulatory regions. For a sample of identified target genes, we show that G-quadruplex stabilizing ligands can modulate transcription. These results confirm the existence of G-quadruplex structures and their persistence in human genomic DNA. Four independent libraries have been enriched in DNA G-quadruplex structures using a G-quadruplex-specific probe. One genomic input library was sequenced as control. Deep-sequencing of these libraries allowed the mapping of G-quadruplexes on the genome.

2013-05-08 | E-GEOD-45241 | biostudies-arrayexpress

Genome wide localization of Activation induced cytidine deaminase (AID), Spt5, and RNA Polymerase II (PolII) in mouse

Project description:Activation induced cytidine deaminase (AID) initiates antibody gene diversification by creating U:G mismatches. However, AID is not specific for antibody genes. Off-target lesions can activate oncogenes or cause chromosome translocations. Despite its importance in these key transactions little is known about how AID finds its target sites. To examine AID regulation we performed an shRNA screen. We found that Spt5, a factor associated with paused RNA polymerase II (Pol II) and single stranded DNA (ssDNA), is required for class switch recombination (CSR). Spt5 interacts with AID, it is required for the association of AID and Pol II, and for AID recruitment to switch regions. ChIP-seq experiments reveal that Spt5 co-localizes with AID and stalled Pol II. Further, Spt5 accumulation at sites of Pol II pausing is predictive of AID-induced mutation. Our data suggest that Spt5 acts as an adaptor, which brings AID to Pol II on target DNA. PolII, AID, and Spt5 were immunoprecipitated from in vitro activated B cells. For Spt5 and AID, two different antibodies were used in separate, biological replicates

2010-10-05 | E-GEOD-24178 | biostudies-arrayexpress

Genome wide localization of Activation induced cytidine deaminase (AID), Spt5, and RNA Polymerase II (PolII) in mouse

2010-10-05 | GSE24178 | GEO

SNP analysis AID-low vs AID-high

Project description:SNP analysis AID-low vs AID-high

2009-07-20 | GSE13612 | GEO

G4 Quadruplex Binding Proteins

Project description:In this study we discover proteins that bind to G4 quadruplex DNA structure. We use modified c-myc quadruplex as a bait, and compare it to the control bait - T15 oligo. We use spectral counts and G-test to determine significant binders. T15 and G4 datafiles are uploaded

2016-07-07 | PXD003501 | Pride

Transcription profiling of mouse AID-GFP-positive vs AID-GFP-negative animals

Project description:Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative Experiment Overall Design: Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

2009-08-22 | E-GEOD-13611 | biostudies-arrayexpress

Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

Project description:Affymetrix gene expression AID-GFP-positive vs AID-GFP-negative

2009-08-15 | GSE13611 | GEO

Rapid degradation of DHX36 revealing its transcriptional role by interacting with G-quadruplex

Project description:More evident supports G-quadruplex are involved in transcription. Recent research revealed that DHX36 preferentially resolves G-quadruplex (G4) structure over the canonical G4, raising the possibility that DHX36 could bind and resolve G4 structures to regulate gene transcription. However, the hypothesis has yet been validated systematically in vivo.In this study, we investigated the role of DHX36 interacting with G4s in transcription. Firstly, we performed CUT&TAG to map the binding sites in chromatin of MCF7. Next, we utilized nascent RNA-seq and AID protein degradation system to identify the direct gene targets by transcriptional regulation of DHX36 and found these sites are enriched with G4 structure. We picked three G4 sequences in oncogene from these sites and found DHX36 binds and resolves these G4 structures in vitro, suggesting DHX36 may be recruited to these promoter G4 sites and regulate gene transcription by resolving G4 structure.

2024-08-13 | GSE228815 | GEO

Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

Project description:Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

| PRJEB32015 | ENA

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