Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Overlapped transcription targets of cGAS and JunB in MDA-MB-231 cells

ABSTRACT: In addition to serving as a cytosolic dsDNA sensor, we found cGAS also participates into transcriptional control on chromatin independent of nucleosomal binding. cGAS is recruited to chromatin by AP-1 factors such as JunB. The goal of this analysis is to determine the common transcriptional targets co-regulated by cGAS and JunB in MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE337117 | GEO | 2026/07/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Overlapped transcription targets of cGAS and JunB in MDA-MB-231 cells

Project description:Overlapped transcription targets of cGAS and JunB in MDA-MB-231 cells

| PRJNA1484078 | ENA

Targeting LYPLAL1-mediated cGAS depalmitoylation enhances the response to anti-tumor immunotherapy

Project description:Cyclic GMP-AMP synthase (cGAS) binds pathogenic and other cytoplasmic double-stranded DNA (dsDNA) to catalyze the synthesis of cyclic GMP-AMP (cGAMP), which serves as the secondary messenger to activate the STING pathway and innate immune responses. Emerging evidence suggests that activation of the cGAS pathway is crucial for anti-tumor immunity, however, no effective intervention method targeting cGAS is currently available. Here we report that cGAS is palmitoylated by ZDHHC9 at cysteines 404/405, which promotes the dimerization and activation of cGAS. We further identified that lysophospholipase-like 1 (LYPLAL1) depalmitoylates cGAS to compromise its normal function. As such, inhibition of LYPLAL1 significantly enhances cGAS-mediated innate immune response, elevates PD-L1 expression and enhances anti-tumor response to PD-1 blockade. Our results therefore reveal that targeting LYPLAL1-mediated cGAS depalmitoylation contributes to cGAS activation, providing a potential strategy to augment the efficacy of anti-tumor immunotherapy.

2024-08-31 | GSE241952 | GEO

Homo sapiens strain:MDA-MB-231

Project description:Evaluation of JunB function in cancer biology

| PRJDB15585 | ENA

Gene induction in STAT1-/- fibroblasts transduced with lentiviruses expressing human cGAS

Project description:The hypothesis tested was that lentiviral driven cGAS expression activates antiviral gene expression. Cells were transduced with lentiviruses expressing cGAS or a control (firefly luciferase). Total RNA was harvested 48 h post-transduction and processed for Illumina BeadArray.

2013-12-01 | E-GEOD-52241 | biostudies-arrayexpress

JUNB ChIP-seq

Project description:JUNB ChIP-seq

| PRJNA802851 | ENA

Activation of cGAS-STING signal to inhibit the proliferation of bladder cancer: the immune effect of cisplatin

Project description:our findings indicated a cisplatin dependent cGAS-STING signal in bladder cancer. This signal could be enhanced by accumulation of dsDNA and chromatin dissociated cGAS and would finally recruit infiltration DCs and CD8+ T cells in bladder cancer bladder cancer tumor microenvironment. However, the specific role and effect of this signal towards bladder cancer tumor microenvironment need to be further clarified.

2021-03-31 | GSE165767 | GEO

cGAS surveillance of micronuclei links genome instability to innate immunity

Project description:DNA is strictly compartmentalised within the nucleus to prevent autoimmunity despite this cGAS, a cytosolic sensor of dsDNA, is activated in autoinflammatory disorders and by DNA damage. Precisely how cellular DNA gains access to the cytoplasm remains to be determined. Here, we report that cGAS localises to micronuclei arising from genome instability in a model of monogenic autoinflammation, after exogenous DNA damage and spontaneously in human cancer cells. These micronuclei occur after mis-segregation of DNA during cell division and consist of chromatin surrounded by their own nuclear membrane. Breakdown of the micronuclear envelope, a process associated with chromothripsis, leads to rapid accumulation of cGAS, providing a mechanism by which self-DNA becomes exposed to the cytosol. cGAS binds to and is activated by chromatin and consistent with a mitotic origin, micronuclei formation and the proinflammatory response following DNA-damage are cell-cycle dependent. Furthermore, by combining live-cell laser microdissection with single cell transcriptomics, we establish that induction of interferon stimulated gene expression occurs in micronucleated cells. We therefore conclude that micronuclei represent an important source of immunostimulatory DNA. As micronuclei formed from lagging chromosomes also activate this pathway, cGAS recognition of micronuclei may act as a cell-intrinsic immune surveillance mechanism detecting a range of neoplasia-inducing processes.

2017-07-24 | GSE100771 | GEO

RNA-Seq of FBXO44 knockdown in MDA-MB-231

Project description:Targeting FBXO44 or SUV39H1 transcriptionally reactivates repetitive elements, triggering RIG-I-MDA5-MAVS and cGAS-STING antiviral defense responses and IFN signaling, specifically in cancer cells

2021-03-26 | GSE139974 | GEO

T cell-intrinsic cGAS-CTCF regulation maintains regulatory T cell development and function [scRNA-Seq]

Project description:Cyclic GMP-AMP synthase (cGAS) is a cytosolic double-strand DNA (dsDNA) sensor in innate immune cells. A function of cGAS is to detect cytosolic double-stranded DNA and synthesize the cyclic dinucleotide 2'3'-cGAMP. This second messenger binds to and activates the adaptor protein STING, triggering the TBK1-IRF3 signaling pathway. However, the function of cGAS in T cells remain unknown and its role in adaptive immunity is also poorly characterized. Here we show that nuclear cGAS promotes regulatory T cell (Treg) development by cooperating with the genome organizer CTCF through a T cell-intrinsic and synthase function-independent way. Conditional deletion of cGAS using Foxp3Cre-YFP Cgasfl/fl and CD4Cre Cgasfl/fl mice demonstrated that cGAS imprints thymocytes for Treg development before the expression of FOXP3. cGAS also promotes the FOXP3 inheritability and suppressive activity of Treg. At steady state, cGAS is located in the nucleus of Treg, while stimulation of naïve CD4+ T cell with anti-CD3/CD28 antibodies induces transcription of cGAS and its translocation into nucleus. ATAC-sequencing of thymic Treg and Treg precursors revealed that CTCF binding is reduced in mature Treg. Mechanistically, cGAS interacts with CTCF and recruits CTCF to Tnfrsf9 (4-1BB) and Tnfrsf4 (OX40) gene locus to maintain their stable transcription through formation of chromatin loops. Physiologically, in mouse tumor model, Treg specific deletion of cGAS reduced tumor growth. Therefore, we uncovered a T cell-intrinsic role of nuclear cGAS in maintaining Treg development and function by imprinting the genome architecture with CTCF.

2025-08-07 | GSE301664 | GEO