Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression during CCK-induced damaged pancreatic acinar cells with or without the addition of OCA

ABSTRACT: Gene expression during CCK-induced damaged pancreatic acinar cells with or without the addition of OCA

PROVIDER: PRJNA1029978 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26440687_1.fastq.gz	Fastqsanger.gz
	SRR26440687_2.fastq.gz	Fastqsanger.gz
	SRR26440688_1.fastq.gz	Fastqsanger.gz
	SRR26440688_2.fastq.gz	Fastqsanger.gz
	SRR26440689_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Gene expression during CCK-induced damaged pancreatic acinar cells with or without the addition of OCA

Project description:Obeticholic acid (OCA) has shown pharmacological protection activity in acinar cell injury and pancreatic necrosis in vitro. RNA sequencing was performed by extracting mRNA from CCK-induced damaged pancreatic acinar cells with or without the addition of OCA. Gene enrichment analysis by Kyoto Encyclopedia of Genes and Genomes (KEGG) identified oxidative phosphorylation in the top ten significantly changed pathways. Similarly, Gene Set Enrichment Analysis (GSEA) enrichment analysis revealed clear alterations in "mitochondrial ATP synthesis coupled electron transport", "mitochondrial respiratory chain complex assembly", "NADH dehydrogenase complex assembly", and "oxidative phosphorylation".

2023-12-31 | GSE245795 | GEO

Zonation of pancreatic acinar cells in diabetic mice

Project description:We sequenced AR42J cell exposed to CCK or insulin in different concentrations. This enable us to uncover the possible effect of the different hormones on acinar cells in pathlogy.

2020-07-17 | GSE154533 | GEO

Evaluation of transcriptional changes of bone marrow derived macrophages (BMDM) in response to necrotic pancreatic acinar cells

Project description:To investigate the activation and polarisation of BMDMs during the course of pancreatitis, BMDMs were co-incubated with CCK-stimulated acinar cells (+/- the serine protease inhibitor nafamostat) for 6h in an in vitro experiment. The LPS treatment served as a positive control.

2022-03-01 | GSE192517 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Relapse scRNAseq]

Project description:The identification of druggable therapeutic targets that preferentially promote autoimmunity remains a key goal in the field. Recent work shows that populations of memory/stem-like T cells drive autoimmunity, but the factors that generate and sustain these populations are incompletely understood. The lymphocyte-restricted transcriptional cofactor OCA-B/Pou2af1 is a regulator of CD4+ T cell memory. Here we show that T cell-intrinsic loss of OCA-B protects mice from experimental autoimmune encephalomyelitis (EAE) in both chronic and relapsing-remitting mouse models while preserving acute responses to infection with a neurotropic coronavirus. In adoptive transfer EAE driven by antigen re-encounter, T cell-specific OCA-B loss largely eliminates Th1- and Th17-mediated CNS infiltration, proinflammatory cytokine production and disease. Using an OCA-B-mCherry reporter mouse, we show that OCA-B expressing CD4+ T cells within the CNS of mice with EAE preferentially display a memory-like phenotype. Transferring these OCA-Bhi memory-like CD4+ T cells preferentially confers disease, identifying OCA-B as a marker of encephalitogenic autoreactive CD4+ T cells. Notably, in a relapsing-remitting EAE model, OCA-B T cell-deficient mice show specific protection at relapse, highlighting the potential to target OCA-B in MS patients to limit disease progression. During remission, OCA-B promotes the expression of Tcf7, Slamf6, and Sell in proliferating T cell populations. At relapse, OCA-B loss results in the accumulation of an immunomodulatory CD4+ T cell population expressing Ccr9 and Bach2. These results highlight OCA-B as a driver of pathogenic stem-like T cells responsible for relapse and promising MS therapeutic target.

2024-04-09 | GSE243724 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Bulk RNAseq]

2024-04-09 | GSE243726 | GEO

OCA-B/Pou2af1 promotes autoimmune demyelination through control of stem-like CD4+ T cells [Remission scRNAseq]

2024-04-09 | GSE243725 | GEO

Targeting OCA-B/Pou2af1 blocks type-1 diabetes and reduces infiltration of activated, islet-reactive T cells

Project description:The transcriptional coregulator OCA-B is induced in stimulated naïve CD4+ T cells, where docks with transcription factor Oct1 to regulate genes such as Il2 and Ifng. OCA-B regulates its targets in cases of repeated antigen exposure, a necessary feature of autoimmunity. Polymorphisms in binding sites for Oct1, and by extension OCA-B, as associated with multiple forms of autoimmunity including autoimmune (type-1) diabetes. We hypothesized that T cell-specific OCA-B deletion would protect mice from type-1 diabetes, and that pharmacologic OCA-B inhibition would provide similar protection. We developed an Ocab (Pou2af1) conditional allele and backcrossed it onto a diabetes-prone NOD/ShiLtJ strain background. T cell-specific OCA-B loss protected mice from spontaneous T1D. To clarify the mechanism, we profiled leukocytes from prediabetic islets by single-cell RNA sequencing and T cell receptor clonotype analysis.

2020-09-29 | GSE145228 | GEO

OCA-T1 and OCA-T2 are coactivators of POU2F3 in the tuft cell lineage

Project description:ChIP-Seq of C11orf53(OCA-T), COLCA2 and POU2F3(OCT11) in tuft cell lung cancer cell lines. Gene expression changes upon CRISPR knockout of different genes in tuft cell lung cancer cell lines and upon over-expression of C11orf53/POU2F3 alone or in combo in YT330 (a murine Notch high small cell lung cancer cell line)

2022-05-01 | GSE186614 | GEO

Transcription profiling of mouse fundic mucosa in the presence/absence of gastrin and in gastrin-CCK double knockout mice

Project description:Fundic mucosa gene expression in wildtype vs gastrin knockout, gastrin replaced gastrin KO and gastrin-CCK double knockout mice; Fundic mucosal scraping RNA were isolated from WT, Gastrin Knockout, Gastrin replaced KO and Gastrin-CCK double knockout mice. Targets from three biological replicates of each were generated and the expression profiles were determined using Affymetrix murine 430A arrays. Comparisons between the sample groups allow the identification of genes with gastrin responsiveness and Gastrin-CCK double effect . Experiment Overall Design: 3 WT, 3 Gastrin KO, 3 Gastrin replaced KO and 3 Gastrin-CCK double Knockout fundic RNA replicates were analyzed

2008-06-13 | E-GEOD-4810 | biostudies-arrayexpress

OCA-T1 and OCA-T2 are coactivators of POU2F3 in the tuft cell lineage

Project description:OCA-T1 and OCA-T2 are coactivators of POU2F3 in the tuft cell lineage

| PRJNA774795 | ENA