Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AID Orchestrates MYC/E2F Target Gene Activation and Cell-of-Origin Transcriptional Programs in Diffuse Large B-cell Lymphoma [GCB_AID-ER_RNA-seq]

ABSTRACT: Activation-induced cytidine deaminase (AID), which is essential for antibody diversification, exhibits elevated expression in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Here, we demonstrate that AID modulates transcriptional programs linked to cell cycle progression, proliferation, and DLBCL subtype identity. AID loss in ABC-type DLBCL cell lines impairs MYC and E2F pathway activity, while AID re-expression restores activity, establishing a causal link. Furthermore, AID expression correlates with ABC-type stratification gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE308039 | GEO | 2026/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

AID Orchestrates MYC/E2F Target Gene Activation and Cell-of-Origin Transcriptional Programs in Diffuse Large B-cell Lymphoma [ABC_AID_KO_RNA-seq]

Project description:Activation-induced cytidine deaminase (AID), which is essential for antibody diversification, exhibits elevated expression in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Here, we demonstrate that AID modulates transcriptional programs linked to cell cycle progression, proliferation, and DLBCL subtype identity. AID loss in ABC-type DLBCL cell lines impairs MYC and E2F pathway activity, while AID re-expression restores activity, establishing a causal link. Furthermore, AID expression correlates with ABC-type stratification gene expression.

2026-03-01 | GSE308037 | GEO

AID Orchestrates MYC/E2F Target Gene Activation and Cell-of-Origin Transcriptional Programs in Diffuse Large B-cell Lymphoma [ABC_AID-ER_RNA-seq]

2026-03-01 | GSE308038 | GEO

CGH data from AID WT vs AID KO BCR-ABL1 mouse leukemia cells

Project description:Activation-induced cytidine deaminase (AID) specific amplifications and deletions in BCR-ABL1 positive Leukemia mouse cells. Bone marrow from Balb/CJ WT and Balb/CJ AID KO mice was transduced with BCR-ABL1. The AID specific amplifications and deletions where analyzed with an Agilent 244A mouse whole Genome CGH Array.

2009-08-15 | GSE15093 | GEO

Gene expression profile for BL2 and BL2 AID-/- cell lines

Project description:AID (activation-induced cytidine deaminase) is expressed at low levels in many tissue types but is most highly expressed in germinal center B cells where it deaminates cytidine to uracil during somatic hypermutation and class switch recombination of the immunoglobulin genes. In addition to this critical role in immune diversification, aberrant targeting of AID contributes to oncogenic point mutations and chromosome translocations associated with B cell malignancies. Thus, to explore a role for AID in DNA demethylation in B cell lymphoma, we performed genome-wide gene expression profiling in BL2 and AID-deficient (AID-/-) BL2 cell lines (Burkitt lymphoma that can be induced to express high levels of AID).

2016-10-01 | GSE85964 | GEO

EBV AID project

Project description:Whole genome sequencing of EBV-transformed B cells in order to determine whether EBV induction of activation-induced cytidine deaminase (AID) produces genome-wide mutations and/or chromosomal rearrangements.

| EGAS00001000955 | EGA

DNA methylation profile for BL2 and BL2 AID-/- cell lines

Project description:AID (activation-induced cytidine deaminase) is expressed at low levels in many tissue types but is most highly expressed in germinal center B cells where it deaminates cytidine to uracil during somatic hypermutation and class switch recombination of the immunoglobulin genes. In addition to this critical role in immune diversification, aberrant targeting of AID contributes to oncogenic point mutations and chromosome translocations associated with B cell malignancies. Thus, to explore a role for AID in DNA demethylation in B cell lymphoma, we performed genome-wide methylation profiling in BL2 and AID-deficient (AID-/-) BL2 cell lines (Burkitt lymphoma that can be induced to express high levels of AID).

2016-11-01 | GSE81215 | GEO

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

Convergent Sense/Antisense Transcription At Intragenic Super-Enhancers Targets AID-initiated Genomic Instability

Project description:Activation-induced cytidine deaminase (AID) initiates both somatic hypermutation (SHM) for antibody affinity maturation and DNA breakage for antibody class switch recombination (CSR) via transcription-dependent cytidine deamination of single stranded DNA targets. While largely specific for immunglobulin genes, AID also acts on a limited set of off-targets, generating oncogenic translocations and mutations that contribute to B cell lymphoma. How AID is recruited to off-targets has been a long-standing mystery. Based on deep GRO-Seq studies of mouse and human B lineage cells activated for CSR or SHM, we report that most robust AID off-target translocations occur within highly focal regions of target genes in which sense and antisense transcription converge. Moreover, we found that such AID-targeting "convergent" transcription arises from antisense transcription that emanates from Super-Enhancers within sense transcribed gene bodies. Our findings provide a mechanistic explanation for AID off-targeting to a small subset of mostly lineage-specific genes in activated B cells. We performed GRO-Seq and H3K27Ac ChIP-Seq with different B lineage cell types and MEF cells to find the signatures associated with AID targeting.

2014-12-04 | E-GEOD-62296 | biostudies-arrayexpress

DNA Methylation Dynamics of Germinal Center B Cells Are Mediated by AID

Project description:Changes in DNA methylation are required for the formation of germinal centers (GC), but the mechanisms of such changes are poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated recently in DNA demethylation through its deaminase activity coupled with DNA repair. We investigated the epigenetic function of AID in vivo in germinal center B cells (GCB) isolated from wild type (WT) and AID-deficient (Aicda-/-) mice. We determined that the transit of B cells through the GC is associated with marked locus-specific loss of methylation and increased methylation diversity, both of which are lost in Aicda-/- animals. Differentially methylated cytosines (DMCs) between GCB and naïve B cells (NB) are enriched in genes that are targeted for somatic hypermutation (SHM) by AID and these genes form networks required for B cell development and proliferation. Finally, we observed significant conservation of AID-dependent epigenetic reprogramming between mouse and human B cells. ERRBS and RNA-seq of wild type and Aicda knockout murine naive and germinal center B cells. ERRBS of human naive and germinal center B cells

2015-09-15 | E-GEOD-71702 | biostudies-arrayexpress

Transcription profiling of AID expressing leukemia and AID deficient leukemia in a mouse model of BCR-ABL1 ALL

Project description:Activation-Induced Cytidine Deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center B lymphocytes. Occasionally, AID targets non-Ig genes, thereby contributing to B cell lymphomagenesis. We recently reported aberrant expression of AID in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL. Mice transplanted with BCR-ABL1-transduced AID-/- bone marrow had prolonged survival as compared to mice transplanted with leukemia cells generated from AID+/+ bone marrow. Consistent with a causative role of AID in genetic instability, AID-/- leukemia had a decreased frequency of amplifications, deletions and a lower frequency of mutations in non-Ig genes including Pax5 and Rhoh as compared to AID+/+ leukemias. AID-/- and AID+/+ ALL cells showed a markedly distinct gene expression pattern as determined by principle component analysis, with 2,365 genes differentially expressed. In contrast to AID+/+ leukemia, AID-/- ALL cells failed to downregulate a number of tumor suppressor genes such as Rhoh, Cdkn1a (p21), and Blnk (SLP65). We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic instability, aberrant somatic hypermutation, and by transcriptional inactivation of tumor suppressor genes. Experiment Overall Design: We used microarrays to detect differences in gene expression profiles between AID expressing leukemia and AID deficient leukemia

2009-07-05 | E-GEOD-16751 | biostudies-arrayexpress

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