Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNAseq ananlysis for CD4+ T cells and monocytes from patients with TRAF6 deficiency.

ABSTRACT: We performed scRNAseq on purified CD4+ T cells and monocytes from age-matched healthy and TRAF6-/- patient cells collected before the treatment to characterize the abnormalities. CD4+ T cells from the TRAF6-/- patient exhibited an activated transcriptome, while examination of the monocytes revealed normal representation of major subsets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE296550 | GEO | 2026/08/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

scRNAseq ananlysis for CD4+ T cells and monocytes from patients with TRAF6 deficiency.

Project description:scRNAseq ananlysis for CD4+ T cells and monocytes from patients with TRAF6 deficiency.

| PRJNA1259960 | ENA

Human blood monocytes scRNAseq

Project description:Human blood monocytes scRNAseq

| PRJNA871108 | ENA

Bluk RNAseq ananlysis for whole blood cells from patients with TRAF6 deficiency.

Project description:Bulk RNAseq was performed for whole blood cells from a TRAF6-/- patient and an age-matched healthy control. The TRAF6-/- patient with lymphoproliferation showed increased T cell transcripts and an enrichment of CD4+ T cell-related markers.

2026-08-27 | GSE296098 | GEO

Human blood monocytes scRNAseq

Project description:scRNAseq of human blood monocytes isolated with magnetic CD14+ beads from two healthy donors.

2022-10-05 | GSE211603 | GEO

scRNAseq of monocytes from Trained immunity experiments

Project description:scRNAseq of monocytes from in vitro Trained immunity experiments stimulated by β-glucan (BG), uric acid (UA), muramyl dipeptide (MDP), oxidized low-density lipoprotein (oxLDL), or RPMI-Control, and respective samples restimulated with Lipopolysaccharide (LPS).

2021-09-30 | E-MTAB-9702 | biostudies-arrayexpress

scRNAseq of monocytes from Trained immunity experiments

Project description:scRNAseq of monocytes from Trained immunity experiments

| PRJEB40999 | ENA

Cytotoxic effects of Bortezomib in Myelodysplastic syndrome/Acute Myeloid Leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1

Project description:Bortezomib (VelcadeM-BM-)) is widely used for the treatment of various human cancers, however, its mechanisms of action are not fully understood, particularly in myeloid malignancies. Bortezomib is a selective and reversible inhibitor of the proteasome. Paradoxically, we find that Bortezomib induces proteasome-independent degradation of TRAF6 protein, but not mRNA, in Myelodysplastic syndrome (MDS) and Acute Myeloid Leukemia (AML) cell lines and primary cells. The reduction in TRAF6 protein coincides with Bortezomib-induced autophagy, and subsequently with apoptosis in MDS/AML cells. RNAi-mediated knockdown of TRAF6 sensitized Bortezomib-sensitive and -resistant cell lines, underscoring the importance of TRAF6 in Bortezomib-induced cytotoxicity. Bortezomib-resistant cells expressing an shRNA targeting TRAF6 were resensitized to the cytotoxic effects of Bortezomib due to down-regulation of the proteasomal subunit alpha-1 (PSMA1). To uncover the molecular consequences following loss of TRAF6 in MDS/AML cells, we applied gene expression profiling and identified an apoptosis gene signature. Knockdown of TRAF6 in MDS/AML cell lines or patient samples resulted in rapid apoptosis and impaired malignant hematopoietic stem/progenitor function. In summary, we describe novel mechanisms by which TRAF6 is regulated through Bortezomib/autophagy-mediated degradation and by which it alters MDS/AML sensitivity to Bortezomib by controlling PSMA1 expression. TF-1 cells were transduced with lentivirus encoding shRNA targeting human TRAF6 and a negative control (pLKO) for 2.5 days. GFP positive cells were sorted for RNA exctration, labeling, and hybridization. A total of four samples were included, and two groups are assigned. Two replicates are for each group. Comparison comprises mRNA expression profile of TRAF6 knockdown (shT6) v.s. control vector (pLKO).

2012-06-14 | E-GEOD-38519 | biostudies-arrayexpress

Trained immunity is facilitated by T cell-induced CD40-TRAF6 signaling [ChIP-seq]

Project description:Trained immunity refers to epigenetic and metabolic changes in innate immune cells following exposure to inflammatory signals, leading to a heightened response to secondary stimuli. Although this innate immune memory contributes to host defense against infections, it can also have maladaptive consequences in a broad range of immune-driven conditions. During the past decade, we have gained an increasingly better understanding of the molecular regulation of trained immunity, but the role of adaptive immune cells in modulation of trained immunity remains largely unknown. Here, we show that T cell interactions contribute to the induction of trained immunity in monocytes and that this mediated by CD40-TRAF6 signaling. Specifically, we found that inhibiting CD40-TRAF6 signaling prevents the induction of functional, transcriptomic, metabolic and epigenetic changes associated with trained immunity. Apart from detailed in vitro studies, we inhibited CD40-TRAF6 signaling in vivo in myeloid cells in a murine heart transplantation model which resulted in prolonged allograft survival. When the animals were additionally treated with costimulatory blockade by CTLA4-Ig, we observed immunological tolerance to the graft. Combined, our study reveals that trained immunity induction is regulated by CD40-TRAF6 signaling between myeloid and adaptive immune cells, and that this signaling can be efficiently leveraged for therapeutic purposes.

2024-08-26 | GSE228182 | GEO

Trained immunity is facilitated by T cell-induced CD40-TRAF6 signaling [RNA-seq]

2024-08-26 | GSE228183 | GEO

Global gene expression in human T cells with targeted disruption of TRAF6 or HOIP

Project description:We profiled gene expression in human CD4 T cells with CRISPR disruptions of TRAF6 or HOIP. The dataset captures transcriptional outputs linked to CBM-proximal ubiquitin signaling and MALT1 activity, enabling comparison of TCR- and TNFR-driven responses and providing a resource to study how distinct E3 ligases shape NF-κB–related programs.

2025-10-11 | GSE299874 | GEO

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