Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cytokine Stimulation of PTPN2-deleted cancer cells

ABSTRACT: PTPN2 was deleted from a selection of murine and human cancer cells using CRISPR/Cas9. The loss-of-function phenotype was assessed in vitro with cytokine stimulation or vehicle control.

OTHER RELATED OMICS DATASETS IN: PRJNA388068

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE99299 | GEO | 2017/07/31

SECONDARY ACCESSION(S): PRJNA388068

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Cytokine Stimulation of PTPN2-deleted cancer cells

Project description:Cytokine Stimulation of PTPN2-deleted cancer cells

| PRJNA388068 | ENA

Cytokine Stimulation of ADAR-deleted B16 murine melanoma cells

Project description:ADAR was deleted from the B16 murine melanoma line using CRISPR/Cas9. The loss-of-function phenotype was assessed in vitro with cytokine stimulation or vehicle control.

2018-12-30 | GSE110708 | GEO

Differential gene expression in WT mice and mice lacking PTPN2 in T cells

Project description:WT mice and mice lacking PTPN2 in T cells (PTPN2-CD4Cre mice) were treated with AOM/DSS to induce colorectal tumours. RNA was isolated from tumour and non-tumour tissues in the colon. Colon samples from water-treated WT and PTPN2-CD4Cre mice served as additional control. Total RNA was isolated and the samples sequenced for polyA enriched RNA.

2020-10-03 | E-MTAB-9629 | biostudies-arrayexpress

PTPN2 knockout vs WT

Project description:We generated pluripotent stem cells (Mel1 hESC containing a GFP reporter driven by the endogenous insulin promoter) with a functional knock out of PTPN2 by CRISPR/Cas9 genome editing. KO or WT control stem cells were differentiated into beta-like cells (sBC), sorted for GFP, and prepared for deep sequencing.

2022-11-30 | GSE211636 | GEO

Cytokine Stimulation of ADAR-deleted B16 murine melanoma cells

Project description:Cytokine Stimulation of ADAR-deleted B16 murine melanoma cells

| PRJNA434332 | ENA

Targeting PTPN2 enhances human CAR T cell efficacy and the development of long-term memory [RNA-seq]

Project description:CAR T cells have been ineffective against solid tumors, where the hostile tumor microenvironment limits CAR T cell function and persistence. Here we have used CRISPR/Cas9 gene-editing, or a small molecule inhibitor to target protein tyrosine phosphatase N2 (PTPN2) in human CAR T cells specific for the Lewis Y (LeY) neo-antigen. Targeting PTPN2 increased CAR and cytokine signaling and enhanced the activation and cytotoxicity of anti-LeY CAR T cells. The deletion or the systemic inhibition of PTPN2 in human CAR T cells repressed the growth of human tumor xenografts or patient-derived xenografts in mice and prolonged survival. PTPN2 deletion or inhibition promoted the generation and intratumoral accumulation of stem cell memory CD8+ CAR T cells that are associated with persistent CAR T cell-mediated tumor repression and improved clinical outcomes in patients. These findings support the use of gene-editing or small molecule inhibitors for targeting PTPN2 in human CAR T cells to combat solid tumors.

2025-10-04 | GSE309442 | GEO

Targeting PTPN2 enhances human CAR T cell efficacy and the development of long-term memory [scRNA-Seq]

2025-10-04 | GSE309443 | GEO

PTPN2 regulates metabolic flux to affect beta cell susceptibility to inflammatory stress

Project description:Protein tyrosine phosphatase N2 (Ptpn2) is a type 1 diabetes (T1D) candidate gene identified from human genome-wide association studies. PTPN2 is highly expressed in human and murine islets and becomes elevated upon inflammation, suggesting that PTPN2 may be important for beta cell survival in the context of T1D. To test whether PTPN2 contributed to beta cell dysfunction in an inflammatory environment, we generated a beta cell-specific deletion of Ptpn2 in mice (Ptpn2 βKO). While unstressed animals exhibit normal metabolic profiles, streptozotocin (STZ) Ptpn2 βKO mice display marked increase in hyperglycemia and death due to exacerbated beta cell loss. Furthermore, cytokine treated Ptpn2 KO islets resulted in mitochondrial defects and reduced glucose-induced metabolic flux, suggesting beta cells lacking Ptpn2 are more susceptible to inflammatory stress associated with T1D due to compromised metabolic fitness.

2023-12-01 | GSE215852 | GEO

HDX-MS analysis of PTPN2 with the CRBN/DDB1 complex

Project description:We used HDX-MS analysis to analyze the interaction between PTPN2 with a compound both in the presence and absence of the CRBN/DDB1 complex. We identified significant changes in HDX when PTPN2 was in the presence of compound. We also identified significant changes when comparing the deuteration profiles of PTPN2 in the presence of compound with and without the CRBN/DDB1 complex.

2024-08-23 | PXD053867 | Pride

RNA sequencing of control and PTPN2 knocked down transcriptomes in EndoC- H1 cells with or without the treatment of pro-inflammatory cytokines

Project description:Type 1 diabetes (T1D) results from autoimmune destruction of β-cells in the pancreas. Protein tyrosine phosphatases (PTPs) are candidate genes for T1D and play a key role in autoimmune disease development and β-cell function. Here, we assessed the global protein and individual PTP profile in the pancreas from diabetic NOD mice treated with anti-CD3 monoclonal antibody and IL-1 receptor antagonist (IL-1RA). The treatment reversed hyperglycemia compared to the anti-CD3 alone control group. We observed enhanced expression of PTPN2, a T1D candidate gene, and endoplasmic reticulum (ER) chaperones in islets from mice with reversed diabetes. To address the functional role of PTPN2 in β-cells, we generated PTPN2 deficient stem cell-derived β-like and human EndoC-βH1 cells. Mechanistically, we demonstrated that PTPN2 inactivation in β-cells exacerbates the type I and type II IFN signalling networks, and the potential progression towards autoimmunity. Moreover, we established the capacity of PTPN2 to modulate the Ca2+-dependent unfolded protein response in β-cells. Adenovirus-induced overexpression of PTPN2 decreased BiP expression and partially protected from ER-stress induced β-cell death. Our results postulate PTPN2 as a key protective factor in β-cells during inflammation and ER stress in autoimmune diabetes.

2022-01-21 | GSE172148 | 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