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Effect of CHOP deficicncy of PTPMT1KO regulatory T cells

ABSTRACT: CD4 T cells were isolated from Wt, PTPMT1 DT, CHOP KO and PTPMT1 DT CHOP DKO mice. Cells were activated in vitro and differentiated into regulatory T cells for 4 days. At this time point cells were harvested and analysed by proteomics.

ORGANISM(S): Mus musculus

PROVIDER: GSE314259 | GEO | 2026/03/25

REPOSITORIES: GEO

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Effect of PTPMT1 deficiency on regulatory T cells

Project description:CD4 T cells were isolated from Wt and PTPMT1 DT mice. Cells were activated in vitro and differentiated into regulatory T cells for 4 days. At this time point WT and KO cells were harvested and analysed by proteomics.

2026-03-25 | GSE288709 | GEO

ER stress time course (WT vs CHOP-/-)

Project description:Primart mouse embryonic fibroblasts (pass 3 to 4) were treated with tunicamycin (2 micrograms/ml) for specified times - genotypes were WILDTYPE and CHOP-/-. Each time point n=4 Keywords: ordered

2004-12-17 | GSE2082 | GEO

Transcription profiling of mouse embryonic fibroblasts (MEF) from wild type vs CHOP-/- genotypes treated with tunicamycin reveals CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

Project description:Primary mouse embryonic fibroblasts (pass 3 to 4) were treated with tunicamycin (2 micrograms/ml) for specified times - genotypes were WILDTYPE and CHOP-/-. Each time point n=4. C/EBP homologous protein CHOP is activated by ER stress, and CHOP deletion protects against its lethal consequences.

2007-12-11 | E-GEOD-2082 | biostudies-arrayexpress

Microarray to find CHOP dependent genes in response to proteasome inhibition

Project description:Environmental stresses that disrupt protein homeostasis induce phosphorylation of eIF2, triggering repression of global protein synthesis coincident with preferential translation of ATF4, a transcriptional activator of the Integrated stress response (ISR). Depending on the extent of protein disruption, ATF4 may not be able to restore proteostatic control and instead switch to a terminal outcome that features elevated expression of the transcription factor CHOP (GADD153/DDIT3). The focus of this study was to define the mechanisms by which CHOP directs gene regulatory networks that determine cell fate. We find that in response to proteasome inhibition, CHOP induces the expression of a collection of genes encoding transcription regulators, including ATF5, which is preferentially translated during eIF2 phosphorylation. Transcriptional expression of ATF5 is directly activated by both CHOP and ATF4. Knock-down of ATF5 increased cell survival in response to proteasome inhibition, supporting the idea that both ATF5 and CHOP have pro-apoptotic functions. Transcriptome analyses of ATF5-dependent genes revealed targets involved in apoptosis, including, NOXA, which is important for inducing cell death during proteasome inhibition. This study suggests that the ISR features a feed-forward loop of stress induced transcriptional regulators, each subject to transcriptional and translational control that can switch cell fate towards apoptosis. 8 plates (10cm) of WT and and 8 plates (10cm) of CHOP-/- MEF cells were subject to no stress (4 each for a total of 8) or treated for 8 hours with 1uM MG132 (4 each for a total of 8). Unstressed cells were harvested at the same time as the stressed cells

2013-09-05 | E-GEOD-43713 | biostudies-arrayexpress

eMERGE Pediatric Studies at CHOP

Project description:eMERGE Pediatric Studies at CHOP

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CHOP ARDS Transcriptomic Subtypes (CATS)

Project description:CHOP ARDS Transcriptomic Subtypes (CATS)

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Proteomic dataset of Wt, PTPMT1 KO, CHOP KO and PTPMT1 CHOP double KO regulatory T cells

Project description:Mitochondrial defects are emerging as key drivers of gut inflammation, colitis, and IBD. Yet, their role in regulating immune tolerance, fine-tuned by helper T cells, is unclear. Understanding how metabolic changes in T cells impact gut tolerogenic mechanisms, including gut colonization and the balance between tolerance and disease, remains, therefore, a critical challenge. Here, we show that cardiolipin deficiency impairs tolerance to Helicobacter due to loss of regulatory T (Treg) cell function. Without cardiolipin, Treg cells lose metabolic fitness and immunosuppressive capacity igniting inflammation, particularly in the gut. Hence, mice with a T cell-specific deletion of the enzyme PTPMT1, essential for cardiolipin synthesis, are highly vulnerable to pathobiont infections even without microbiome imbalance. Notably, patients affected by Barth syndrome, a genetic disease characterized by severe cardiolipin deficiency, also exhibit inflammation and helper T cell imbalance. Overall, we found that cardiolipin in T cells preserves gut-immune homeostasis, dictating outcomes in pathobiont infections.

2026-04-14 | PXD071483 | Pride

FUS-CHOP and ISWI chromatin remodeling in human myxoid liposarcoma

Project description:We identified novel protein-protein interactions between FUS-CHOP, a fusion oncoprotein that drives myxoid liposarcoma, and SNF2H, the ATPase subunit of the imitation switch (ISWI) chromatin remodeling complex. We used antibodies for FUS-CHOP, SNF2H, and H3K27ac to profile localization of these proteins and histones marks on chromatin in human MLPS cell lines and show that colocalization of FUS-CHOP and SNF2H occurs at new enhancers marked by H3K27ac.

2022-02-21 | GSE145678 | GEO

TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma

Project description:MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. Thus we explored the target microRNA of TLS-CHOP influence cell-proliferation or cell death with microarray. MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. In this study, we have found that miR-486-5p (miR-486) expression level was downregulated by ectopic expression of TLS-CHOP fusion gene in mouse fibroblast cells (NIH3T3). In addition, we found overexpression of miR-486 inhibited the cell growth in the 2645/94 cells and in situ hybridization of miR-486 showed MLS tissues had lower signal intensity compared with non-tumor tissues. Thus we explored the target genes of miR-486 influence cell-proliferation or cell death with microarray. We compared the microRNA profiles of cells treated with TLS-CHOP or empty vector about NIH-3T3 cell-line. We compared the whole mRNA profiles of cells transfected with miR-486 oligonucleotides or control oligo about myxoid liposarcoma cell-line.

2013-03-23 | E-GEOD-36966 | biostudies-arrayexpress

Transcription profiling of human patients with diffuse large B-cell lymphoma treated with CHOP or Ritxumab-CHOP

Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). 53 samples hybridized on Affymetrix HG-U133A GeneChips arrays, for 53 patients with diffuse large B-cell lymphoma (DLBCL); patients are treated with CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone) or Ritxumab (R)-CHOP in the Groupe dB^REtude des Lymphomes de lB^RAdulte (GELA) clinical centers.

2008-06-01 | E-TABM-346 | biostudies-arrayexpress

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