Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EGR2 O-GlcNAcylation Orchestrates the Development of Protumoral Macrophages to Limit CD8+ T Cell Antitumor Responses.

ABSTRACT: EGR2 O-GlcNAcylation Orchestrates the Development of Protumoral Macrophages to Limit CD8+ T Cell Antitumor Responses.

PROVIDER: PRJNA1156578 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR30542737_1.fastq.gz	Fastqsanger.gz
	SRR30542737_2.fastq.gz	Fastqsanger.gz
	SRR30542739_1.fastq.gz	Fastqsanger.gz
	SRR30542739_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 39

Similar Datasets

EGR2 O-GlcNAcylation Orchestrates the Development of Protumoral Macrophages to Limit CD8+ T Cell Antitumor Responses

Project description:ETD-based LC-MS/MS analysis was used for Identification of transcription factor EGR2 O-GlcNAcylation sites

2025-05-09 | PXD063792 |

EGR2 O-GlcNAcylation Orchestrates the Development of Protumoral Macrophages to Limit CD8+ T Cell Antitumor Responses.

Project description:Tumor associated macrophages (TAMs) exihibit a high capacity to take up glucose, however, how metabolic cues derived from glucose uptake rewire TAMs remains unclear. Here, we report that glucose metabolism-driven protein O-GlcNAcylation shapes the differentiation of protumoral TAMs, thereby accelerating tumor progression. We constructed O-GlcNAc transferase (OGT) conditional-deletion mice to examine MC38 tumor growth.

2025-06-10 | GSE276300 | GEO

RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

Project description:Transcription profiling of mouse FR4+Egr2+, FR4+Egr2- and FR4-Egr2- CD4+ T cells extracted from GFP-Egr2 knockin (Egr2 Kin) and FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4+ T cells isolated from Egr2loxP/loxP hCD2-Cre Egr3-/- (Egr2/3 DKO) mice in the steady state or 21 days after infection with vaccinia virus.

2025-01-01 | E-MTAB-12736 | biostudies-arrayexpress

RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

Project description:RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

| PRJEB60459 | ENA

GlcNAcylation of histone H2B facilitates its monoubiquitination

Project description:This SuperSeries is composed of the following subset Series: GSE33049: GlcNAcylation of histone H2B facilitates its monoubiquitination [Illumina Genome Analyzer data] GSE33050: GlcNAcylation of histone H2B facilitates its monoubiquitination [Affymetrix data] Refer to individual Series

2011-10-26 | E-GEOD-33051 | biostudies-arrayexpress

GlcNAcylation of histone H2B facilitates its monoubiquitination [Illumina Genome Analyzer data]

Project description:We report that histone GlcNAcylation of H2B S112 is a vital histone modification which facilitates histone monoubiquitination (ub). In a genome-wide analysis, H2B S112 GlcNAcylation sites were observed widely distributed over entire chromosomes including transcribed gene loci, together with co-localization of H2B S112 GlcNAcylation and K120 ub. Examination of H2B S112 GlcNAc and H2B K120 ub in HeLa S3 cells

2011-10-27 | E-GEOD-33049 | biostudies-arrayexpress

O-GlcNAcylation of FOXK1 orchestrates the E2F pathway

Project description:Gene transcription is a highly regulated process, and deregulation of transcription factors activity underlie numerous pathologies including cancer. FOXK1 and FOXK2 (FOXK1/2) transcription factors have recently emerged as important regulators of cell metabolism, autophagy and cell differentiation. While FOXK1/2 possesses many overlapping functions in normal biology, their specific functions as well as deregulation of their transcriptional activity in cancer is less clear and often contradictory. FOXK1, but less FOXK2, is known to have oncogenic properties as higher expression levels of FOXK1 has been observed in several cancers and is correlated with tumor progression, invasion, and metastasis. However, the molecular mechanism by which FOXK1 exert its oncogenic properties in caner remains unknown. Here we show that elevated expression of FOXK1, but not FOXK2, in normal human fibroblasts promotes transcription of E2F target genes associated with increased proliferation and delayed senescence entry. Fibroblasts overexpressing FOXK1 are also more prone to cellular transformation with minimal oncogenic combinations, suggesting important oncogenic proprieties of FOXK1. Mechanistically, we found that FOXK1, but not FOXK2, is specifically modified by O-GlcNAcylation. FOXK1 O-GlcNAcylation is modulated during the cell cycle and its highest levels coincides with the G1/S phase transition. Moreover, FOXK1 O-GlcNAcylation is increased following cell transformation and loss of this modification leads to decreased FOXK1 ability to promote cellular transformation and tumor growth. Cells overexpressing FOXK1 O-GlcNAcylation-defective mutants have lower E2F1 expression, cell proliferation, and tumour growth. Our results define a distinct role of FOXK1 via O-GlcNAcylation in controlling the cell cycle through the orchestration of the E2F pathway.

2024-06-10 | PXD050014 | Pride

GFP-Egr2 ChIP-seq analysis of CD4 T cells

Project description:Identification of Egr2 binding sites in CD4 T cells from GFP-Egr2 knockin (Egr2 Kin) mice by GFP-Egr2 ChIP-seq

2020-07-19 | E-MTAB-7797 | biostudies-arrayexpress

Type I Interferon Signaling via the EGR2 Transcriptional Regulator Potentiates CAR T cell-intrinsic Dysfunction (RNA-Seq)

Project description:Chimeric antigen receptor (CAR) T-cell therapy has achieved remarkable success in the treatment of hematopoietic cancers, but resistance is common, and efficacy is limited in solid tumors. We demonstrate that CAR T-cells autonomously propagate epigenetically-programmed type I interferon signaling through chronic stimulation or antigen-independent tonic activation, which progressively hampers antitumor effector function. EGR2 transcriptional regulator knockoutnot only blocks this type I interferon-mediated inhibitory program, but also independently expands early memory CAR T-cells with improved efficacy against liquid and solid tumors. The protective effect of EGR2 deletion in CAR T-cells against chronic antigen-induced dysfunction can be overridden by interferon-β exposure, suggesting that EGR2 ablation suppresses CAR T-cell dysfunction through inhibition of type I interferon signaling. Finally, enrichment of an EGR2 gene signature is a clinical biomarker for type I interferon-associated CAR T-cell failure and shorter overall patient survival. These findings conceptually connect prolonged CAR T-cell activation with deleterious immunoinflammatory signaling and point to an EGR2-type I interferon axis as a therapeutically amenable biologic system.

2023-02-20 | GSE224193 | GEO

Type I Interferon Signaling via the EGR2 Transcriptional Regulator Potentiates CAR T cell-intrinsic Dysfunction (ATAC-Seq)

2023-02-20 | GSE224192 | GEO