Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

49 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq of explanted murine pancreatic acinar cells

ABSTRACT: To investigate the underlying changes during acinar-to-ductal metaplasia, pancreatic acinar cells were isolated from 5 week old KrasG12D-mice. RNA was isolated immediately after isolation (t=0 days) or after 3 days embedded in collagen.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Henrik Einwächter

PROVIDER: E-MTAB-9878 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-Seq of explanted murine pancreatic acinar cells from wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia induced by different factos, pancreatic acinar cells were isolated from 5 week old wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice. Acinar cells from wt mice were treated with medium (control), Tgfa or IL17a. RNA was isolated immediately after isolation (t=0 days) or after 2-3 days embedded in collagen.

2024-05-31 | E-MTAB-11913 | biostudies-arrayexpress

RNA-seq of mouse cell lines isolated from genetically engineered mouse models of extrahepatic cholangiocarcinoma and pancreatic cancer

Project description:Biliary tract cancer (BTC) ranks among the most lethal human malignancies, thereby representing an unmet clinical need. In this study, we find that the Pdx1-positive extrahepatic biliary epithelium is highly susceptible towards transformation by activated Pik3caH1047R, but completely refractory to oncogenic KrasG12D. Using genome-wide in vivo piggyBac transposon-based forward genetic screening and genetic loss-of-function experiments, we discover important extrahepatic cholangiocarcinoma (ECC) cancer genes and find that PI3K-signaling output strength and repression of the tumor suppressor p27Kip1 are critical context-specific determinants of tumor formation. This contrasts the pancreas, where oncogenic Kras in concert with Trp53 loss of function are key cancer drivers. Notably, inactivation of p27Kip1 permits KrasG12D-driven ECC development, and bypasses oncogene-induced senescence without triggering the Trp53 pathway. These studies provide a mechanistic link between PI3K-signaling, tissue-specific tumor suppressor barriers, and ECC pathogenesis, and present a novel genetic model of autochthonous ECC and genes driving this highly lethal tumor-subtype.

2021-07-05 | E-MTAB-10515 | biostudies-arrayexpress

RNA-seq of pancreatic mouse tumor cell lines

Project description:KRAS-mutant pancreatic ductal adenocarcinoma (PDAC) is highly immunosuppressive and resistant to targeted therapies, immune checkpoint blockade and engineered T cells. In this study, we performed a systematic high throughput combinatorial drug screen and identified a synergistic interaction between the MEK inhibitor trametinib and the multi-kinase inhibitor nintedanib. Using bulk and single-cell RNA sequencing and immunophenotyping, we show that the combination therapy reprograms the immunosuppressive microenvironment and primes cytotoxic and memory T cells to infiltrate the tumors, thereby sensitizing mesenchymal PDAC to PD-L1 inhibition.

2021-11-29 | E-MTAB-11187 | biostudies-arrayexpress

RNA-Seq of pancreatic tissue from wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice, at 10 weeks and after induction of acute pancreatitis

Project description:To investigate the underlying changes during acinar-to-ductal metaplasia induced by different oncogenes and by acute pancreatitis, pancreatic tissue was isolated from 10 week old control wt, KrasG12D, Pi3kCAH1047R and Mek1dd mice and from mice of the same genotypes after induction of acute pancreatitis.

2024-04-06 | E-MTAB-13946 | biostudies-arrayexpress

Epigenetic reprogramming in pancreatic acinar cell in the absence of MIST1

Project description:Epigenetic profile of tissues is reprogrammed under diseased conditions. H3K4Me3 and H3K27Me3 represent active and repressive epigenetic marks, respectively. ChIP-seq is an effective tool to study global protein-DNA interactions. To study global epigenetic differences, we used H3K4Me3 antibody to evaluate its enrichment in pancreatic acinar cells of WT and Mist1-/- mice followed by next generation sequencing. We found specific hotspots that showed differential enrichment for H3K4Me3 both in WT and Mist1-/- mice. The data show that pancreatic acinar cells are epigenetically reprogrammed under stressed cellular conditions. Global H3K4Me3 profiling of WT and Mist1-/- pancreatic acinar cells using ChIP-seq.

2014-07-21 | E-GEOD-49113 | biostudies-arrayexpress

Transcriptional program for induced delta cell on day10

Project description:Direct lineage conversion of adult cells is a promising approach for regenerative medicine. A major challenge of lineage conversion is to generate specific subtypes of cells, closely related cells with distinct properties. The pancreatic islets contain three major hormone-secreting endocrine subtypes: insulin+ β-cells, glucagon+ α-cells, and somatostatin+ δ-cells. We previously reported that a combination of three transcription factors, Ngn3, Mafa, and Pdx1, directly reprogram pancreatic acinar cells to β-cells. We now show that acinar cells can be converted to δ-like and α-like cells by Ngn3 and Ngn3+Mafa respectively. Thus, three major islet endocrine subtypes can be derived by acinar reprogramming. Ngn3 promotes establishment of a generic endocrine state in acinar cells at the onset of reprogramming in addition to promoting δ-specification. Mafa and Pdx1 suppress δ-specification in α- and β-cell formation. These studies identify a set of defined factors whose combinatorial actions reprogram acinar cells to distinct islet endocrine subtypes in vivo. induced beta cells samples at day 10 collected for the microarray

2013-11-20 | E-GEOD-52522 | biostudies-arrayexpress

Transcriptional and epigenetic program changes of induced beta cells over time [RRBS-seq]

Project description:Direct lineage conversion is a promising approach to generate therapeutically important cell types for disease modeling and tissue repair. However, it is often unclear whether lineage-reprogrammed cells remain stable long-term and whether the properties of the reprogrammed cells evolve over time. Here, using an improved method of converting pancreatic acinar cells to beta-cells, we show that induced beta-cells persist in the adult pancreas for up to 14 months and form islet-like structures. Detailed analyses of induced cells over 7 months reveal that global DNA methylation changes occur rapidly whereas transcription network remodeling evolves over two months to resemble that of endogenous beta-cells and then stabilizes thereafter. Progressive gain of beta-cell function by converted cells during the 7 month period coincides with both transcriptional changes and the formation of islet-like structures. These studies demonstrate the ability of lineage-reprogrammed cells to achieve a stable state and identify key cellular and molecular milestones during their long-term evolution. Acinar cells and beta cells were collected as control, as well as induced beta cell samples at day 10, day 30, day 60, and 7 months

2014-11-15 | E-GEOD-59615 | biostudies-arrayexpress

Analysis of thymic dendritic cells (DCs) subtypes from Foxn1cre x ROSA26TdTOMATO mice by single cell transcription profiling.

Project description:Thymi from Foxn1cre x ROSA26TdTOMATO were enzymaticaly digested, cells were MACS enriched for CD11c+ fraction. Dendritic cells were then FACS sorted (BD influx sorter) as Gr-1-CD11c+TdTOMATO+. TdTOMATO DCs represent fraction of thymic DCs which acquire antigen (TdTOMATO) from thymic epithelial cells, through the process of antigen transfer.

2020-03-20 | E-MTAB-8028 | biostudies-arrayexpress

Proteogenomic characterization of pancreatic acinar cell carcinoma and pancreatoblastoma

Project description:To characterize pancreatic cancer with acinar differentiation at protein level, we performed mass spectromery-based proteome analysis using clinical FFPE tissue samples.

2024-09-17 | PXD036998 | Pride

Inhibition of ketohexokinase C isoform impairs the development of PDAC tumors

Project description:the genetic inactivation of Khk-C enhanced the survival of KPC-driven PDAC model even in absence of high fructose diet. Moreover Khk-C knock out decreased the viability of KPC organoids and cancer cells, the migratory capability of PDAC cells in vitro and the growth of KPC cells in vivo in a cell autonomous manner.

2023-07-07 | E-MTAB-12746 | biostudies-arrayexpress

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