Cytokine Stimulation of PTPN2-deleted cancer cells
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA388068
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE99299 | GEO | 2017/07/31
SECONDARY ACCESSION(S): PRJNA388068
REPOSITORIES: GEO
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Project description:Cytokine Stimulation of PTPN2-deleted cancer cells
| PRJNA388068 | ENA
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
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
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
Project description:Cytokine Stimulation of ADAR-deleted B16 murine melanoma cells
| PRJNA434332 | ENA
Project description:Background: Protein tyrosine phosphatases (PTPs) play key roles in b-cell function and diabetes development. PTPN2 is a candidate gene for type 1 diabetes (T1D) that negatively regulates the JAK/STAT signaling. However, the impact of PTPN2 deficiency on the differentiation and functionality of human stem cell-derived somatic metabolic cells remains unclear. Methods: PTPN2 expression in b cells from T1D organ donors and during the differentiation of human stem cell-derived islets (SC-islets) was evaluated in single-cell RNA-Sequencing data. Moreover, we differentiated CRISPR-Cas12a genome-edited PTPN2-deficient H1 human embryonic stem cells (H1-hESCs) into SC-islets, and sc RNA-Seq was performed. The maturation and functionality PTPN2 deficient SC-islets were assessed by implantation under the kidney capsule of NOD-SCID mice. Results: scRNA-Seq analysis showed that PTPN2 expression was increased in b cells from recently diagnosed T1D and decreased in long-standing T1D organ donors, compared with controls. Conversely, we found that PTPN2 expression was decreased at early stages of SC-islet differentiation and reconstituted at later stages, suggesting a developmental dynamic. CRISPR/Cas12-mediated gene editing was used to generate PTPN2-knockout human embryonic stem cells. PTPN2 deficiency exacerbated interferon-induced inflammatory signaling in stem cells and differentiated somatic metabolic cells. Interestingly, PTPN2 deficiency increased hedgehog signaling and reduced SC-islet differentiation efficiency in vitro. In addition, PTPN2-knockout SC-islets exhibited reduced glycemic control after implantation in vivo, mediated by reduced cell endocrine identity and enhanced interferon signaling. Conclusions: Our study postulates a key role of PTPN2 in preserving b-cell function during inflammatory and metabolic stress in SC-islets.
2026-03-18 | GSE304008 | GEO
Project description:Background: Protein tyrosine phosphatases (PTPs) play key roles in b-cell function and diabetes development. PTPN2 is a candidate gene for type 1 diabetes (T1D) that negatively regulates the JAK/STAT signaling. However, the impact of PTPN2 deficiency on the differentiation and functionality of human stem cell-derived somatic metabolic cells remains unclear. Methods: PTPN2 expression in b cells from T1D organ donors and during the differentiation of human stem cell-derived islets (SC-islets) was evaluated in single-cell RNA-Sequencing data. Moreover, we differentiated CRISPR-Cas12a genome-edited PTPN2-deficient H1 human embryonic stem cells (H1-hESCs) into SC-islets, and sc RNA-Seq was performed. The maturation and functionality PTPN2 deficient SC-islets were assessed by implantation under the kidney capsule of NOD-SCID mice. Results: scRNA-Seq analysis showed that PTPN2 expression was increased in b cells from recently diagnosed T1D and decreased in long-standing T1D organ donors, compared with controls. Conversely, we found that PTPN2 expression was decreased at early stages of SC-islet differentiation and reconstituted at later stages, suggesting a developmental dynamic. CRISPR/Cas12-mediated gene editing was used to generate PTPN2-knockout human embryonic stem cells. PTPN2 deficiency exacerbated interferon-induced inflammatory signaling in stem cells and differentiated somatic metabolic cells. Interestingly, PTPN2 deficiency increased hedgehog signaling and reduced SC-islet differentiation efficiency in vitro. In addition, PTPN2-knockout SC-islets exhibited reduced glycemic control after implantation in vivo, mediated by reduced cell endocrine identity and enhanced interferon signaling. Conclusions: Our study postulates a key role of PTPN2 in preserving b-cell function during inflammatory and metabolic stress in SC-islets.
2026-03-18 | GSE303371 | GEO
Project description:Background: Protein tyrosine phosphatases (PTPs) play key roles in b-cell function and diabetes development. PTPN2 is a candidate gene for type 1 diabetes (T1D) that negatively regulates the JAK/STAT signaling. However, the impact of PTPN2 deficiency on the differentiation and functionality of human stem cell-derived somatic metabolic cells remains unclear. Methods: PTPN2 expression in b cells from T1D organ donors and during the differentiation of human stem cell-derived islets (SC-islets) was evaluated in single-cell RNA-Sequencing data. Moreover, we differentiated CRISPR-Cas12a genome-edited PTPN2-deficient H1 human embryonic stem cells (H1-hESCs) into SC-islets, and sc RNA-Seq was performed. The maturation and functionality PTPN2 deficient SC-islets were assessed by implantation under the kidney capsule of NOD-SCID mice. Results: scRNA-Seq analysis showed that PTPN2 expression was increased in b cells from recently diagnosed T1D and decreased in long-standing T1D organ donors, compared with controls. Conversely, we found that PTPN2 expression was decreased at early stages of SC-islet differentiation and reconstituted at later stages, suggesting a developmental dynamic. CRISPR/Cas12-mediated gene editing was used to generate PTPN2-knockout human embryonic stem cells. PTPN2 deficiency exacerbated interferon-induced inflammatory signaling in stem cells and differentiated somatic metabolic cells. Interestingly, PTPN2 deficiency increased hedgehog signaling and reduced SC-islet differentiation efficiency in vitro. In addition, PTPN2-knockout SC-islets exhibited reduced glycemic control after implantation in vivo, mediated by reduced cell endocrine identity and enhanced interferon signaling. Conclusions: Our study postulates a key role of PTPN2 in preserving b-cell function during inflammatory and metabolic stress in SC-islets.
2026-03-18 | GSE305271 | GEO
Project description:Background: Protein tyrosine phosphatases (PTPs) play key roles in b-cell function and diabetes development. PTPN2 is a candidate gene for type 1 diabetes (T1D) that negatively regulates the JAK/STAT signaling. However, the impact of PTPN2 deficiency on the differentiation and functionality of human stem cell-derived somatic metabolic cells remains unclear. Methods: PTPN2 expression in b cells from T1D organ donors and during the differentiation of human stem cell-derived islets (SC-islets) was evaluated in single-cell RNA-Sequencing data. Moreover, we differentiated CRISPR-Cas12a genome-edited PTPN2-deficient H1 human embryonic stem cells (H1-hESCs) into SC-islets, and sc RNA-Seq was performed. The maturation and functionality PTPN2 deficient SC-islets were assessed by implantation under the kidney capsule of NOD-SCID mice. Results: scRNA-Seq analysis showed that PTPN2 expression was increased in b cells from recently diagnosed T1D and decreased in long-standing T1D organ donors, compared with controls. Conversely, we found that PTPN2 expression was decreased at early stages of SC-islet differentiation and reconstituted at later stages, suggesting a developmental dynamic. CRISPR/Cas12-mediated gene editing was used to generate PTPN2-knockout human embryonic stem cells. PTPN2 deficiency exacerbated interferon-induced inflammatory signaling in stem cells and differentiated somatic metabolic cells. Interestingly, PTPN2 deficiency increased hedgehog signaling and reduced SC-islet differentiation efficiency in vitro. In addition, PTPN2-knockout SC-islets exhibited reduced glycemic control after implantation in vivo, mediated by reduced cell endocrine identity and enhanced interferon signaling. Conclusions: Our study postulates a key role of PTPN2 in preserving b-cell function during inflammatory and metabolic stress in SC-islets.
2026-03-18 | GSE303368 | GEO
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 | GSE309443 | GEO