Similar Datasets
Project description:Pancreatic Differentiation Clones and Pooled Single-cell RNA-seq
| PRJNA1039795 | ENA
Project description:To investigate the role of HHEX in regulating human pancreatic endoderm differentiation, we knocked down the HHEX gene in 585A1 cell line-derived pancreatic endoderm cells by siRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of the 3 cell samples.
2023-01-05 | GSE222068 | GEO
Project description:Pancreatic islet isolation for single-cell RNA sequencing (scRNA-seq) requires extensive enzymatic and mechanical processing that may affect cell recovery and transcriptional state. We evaluated a practical gradient-free workflow for murine pancreatic islets from diabetic BKS.Cg-Dock7^m +/+ Lepr^db/J mice. The protocol combined intraductal collagenase perfusion, controlled digestion, stereomicroscope-guided manual islet selection without density-gradient purification, and gentle Accutase/EDTA dissociation. Compared with Ficoll-based purification, the gradient-free workflow omitted density-gradient preparation, gradient centrifugation, additional wash centrifugations, and associated transfer steps while yielding viable cells suitable for scRNA-seq. The resulting library met the applied QC criteria and retained the major endocrine populations. Stress-associated transcriptional differences between the two pooled libraries were descriptive only. Overall, the gradient-free workflow represents a feasible alternative to Ficoll-based purification for preparing murine pancreatic islets for scRNA-seq.
2026-09-30 | GSE347182 | GEO
Project description:Previous study (Segerstolpe Å et.al., Cell Metab . 2016) has revealed the single-cell landscape of human pancreatic islets from 10 human individuals. Here, we have performed Smart-seq2 scRNA-seq of additional 4 healthy and 6 T2D individuals.
2025-08-22 | GSE214517 | GEO
Project description:MAP4K family kinases are key kinases for T-cell-mediated immune responses; however, in vivo roles of MAP4K2 in immune regulation remain unclear. Using T- cell-specific Map4k2 conditional knockout (T-Map4k2 cKO) mice, single-cell RNA sequencing (scRNA-seq), and mass spectrometry analysis, we found that MAP4K2 interacted with DDX39B, induced FOXP3 gene expression, and promoted Treg differentiation. Mechanistically, MAP4K2 directly phosphorylated the DEAD box protein DDX39B, leading to DDX39B nuclear translocation and subsequent Foxp3 RNA splicing. MAP4K2-induced FOXP3 mRNA levels were abolished in DDX39B knockout T cells. Furthermore, T-Map4k2 cKO mice displayed the reduction of Treg population and sustained inflammation during remission phase of EAE autoimmune disease model. Remarkably, the anti-PD-1 immunotherapeutic effect on pancreatic cancer was drastically improved in T-Map4k2 cKO mice, Treg-specific Map4k2- deficient mice, or MAP4K2-inhibitor-treated mice. Consistently, scRNA-seq analysis of human pancreatic or lung cancer patients showed increased MAP4K2 levels in infiltrating Treg cells. Collectively, MAP4K2 promotes Treg differentiation by inducing DDX39B nuclear translocation, leading to the attenuation of tumor immunity.
2025-12-16 | PXD070831 | Pride
Project description:MAP4K family kinases are key kinases for T-cell-mediated immune responses; however, in vivo roles of MAP4K2 in immune regulation remain unclear. Using T-cell-specific Map4k2 conditional knockout (T-Map4k2 cKO) mice, single-cell RNA sequencing (scRNA-seq), and mass spectrometry analysis, we found that MAP4K2 interacted with DDX39B, induced FOXP3 gene expression, and promoted Treg differentiation. Mechanistically, MAP4K2 directly phosphorylated the DEAD box protein DDX39B, leading to DDX39B nuclear translocation and subsequent Foxp3 RNA splicing. MAP4K2-induced FOXP3 mRNA levels were abolished in DDX39B knockout T cells. Furthermore, T-Map4k2 cKO mice displayed the reduction of Treg population and sustained inflammation during remission phase of EAE autoimmune disease model. Remarkably, the anti-PD-1 immunotherapeutic effect on pancreatic cancer was drastically improved in T-Map4k2 cKO mice, Treg-specific Map4k2-deficient mice, adaptively transferred mice, or MAP4K2-inhibitor-treated mice. Consistently, scRNA-seq analysis of human pancreatic patients showed increased MAP4K2 levels in infiltrating Treg cells. Collectively, MAP4K2 promotes Treg differentiation by inducing DDX39B nuclear translocation, leading to the attenuation of tumor immunity.
2025-12-16 | PXD070940 | Pride
Project description:Primary human pancreatic ductal organoids (HPDO) have emerged as a model to study pancreas biology and model disease like pancreatitis and pancreatic cancer. Yet, donor material availability, genetic variability and a lack of extensive benchmarking to healthy and disease pancreas limits the range of applications. To address this gap, we established porcine pancreatic ductal organoids (PPDO) as a system from a reliable, genetically defined and easily obtainable source to model pancreatic ductal/progenitor biology. We benchmarked PPDO to HPDO and primary porcine pancreas using single-cell RNA sequencing (scRNA-Seq). We observed no overt phenotypic differences in PPDO derived from distinct developmental stages using extensive proteomics profiling, with a WNT/basal cell signaling enriched population characterizing PPDO. PPDO exhibited differentiation potential towards mature ductal cells and limited potential towards endocrine lineages. We used PPDO as a chemical screening platform to assess the safety of FDA-approved drugs and showed conserved toxicity of statins and α-adrenergic receptor inhibitors between PPDO and HPDO cultures. Overall, our results highlight the PPDO as a model for mammalian duct/progenitor applications.
2025-11-10 | PXD068063 | Pride
Project description:GATA6 is a master regulator of differentiation in the pancreas and its expression levels determine the two main molecular subtypes of pancreatic cancer. High GATA6 contributes to the “classical” pancreatic cancer subtype, which is associated with a higher degree of tumor differentiation and better disease prognosis. However, why GATA6 expression varies across pancreatic cancers and what regulate GATA6 expression remain elusive. Here we report that the oncogenic KRAS-activated ERK signaling suppresses GATA6 transcription in pancreatic cancers. GATA6 mRNA levels inversely correlated with KRAS/ERK activity in pancreatic tumors. A genome-wide CRISPR screen in a GATA6-EGFP reporter knockin cell line identified JUNB as the ERK-regulated transcriptional repressor for GATA6. Active ERK stabilizes JUNB protein while KRAS/ERK inhibition led to ubiquitin-independent proteasomal degradation of JUNB and increased transcription of GATA6. Up-regulation of GATA6 enhanced chemosensitivity of pancreatic cancer cells and KRAS/ERK inhibitors synergized with chemotherapy in a GATA6-dependent manner. Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.
2025-11-20 | GSE307506 | GEO
Project description:Single-cell transcriptomic dataset comprising 41 patient-derived cell cultures (PDCs) established from pancreatic ductal adenocarcinoma (PDAC). The dataset was generated using Evercode™ technology with the Whole Transcriptome v2 kit (Parse Biosciences, ECW02130), based on Split Pool Ligation-based Transcriptome sequencing (SPLiT-seq). For scRNA-seq, PDCs were processed in two batches, 14 samples in the first batch (R1) and 27 samples in the second batch (R2). Sequencing was performed separately for each batch using the Illumina NovaSeq X Plus platform. Paired-end reads were generated on a 10B flow cell with 200 sequencing cycles. FASTQ quality control (QC), barcode correction, alignment to the human reference genome (GRCh38.p13), multiplet detection, and raw count matrix generation were performed using the split-pipe pipeline (v1.1.1, Parse Biosciences) with default parameters. This single-cell collection of experimentally derived models reveals transcriptional heterogeneity both within and across PDCs. The submitted file consists of the count matrix along with the corresponding metadata.
2026-04-15 | E-MTAB-16856 | biostudies-arrayexpress
Project description:Single-cell RNA sequencing (scRNA-seq) is a powerful tool for defining cellular diversity in tumors, but its application towards dissecting mechanisms underlying immune-modulating therapies is scarce. We performed scRNA-seq analyses on immune cells in mouse tumors and identified specific macrophage and conventional dendritic cell (cDC) subsets that are comparable to previously described human myeloid populations. Defining comparable myeloid populations in mouse tumors enabled characterization of their response to myeloid-targeted immunotherapy. Treatment with anti-CSF1R selectively depleted macrophages with an inflammatory signature but spared a macrophage population that in mouse and human expresses pro-angiogenic/tumorigenic genes. Treatment with a CD40 agonist antibody preferentially activated of a cDC1-Ccl22 population and gradually increased Bhlhe40+ Th1-like cells and CD8+ memory T cells. Our comprehensive analysis of key myeloid subsets in human and mouse identifies critical cellular interactions regulating tumor immunity and defines mechanisms underlying myeloid-targeted immunotherapies currently undergoing clinical testing. Raw FASTQ sequences have been uploaded to European Nucleotide Archive (Study #: PRJEB34105 (ERP116961))
2020-02-23 | E-MTAB-8832 | biostudies-arrayexpress