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Bulk RNA-Seq comparing pancreatic acinar cells expressing KRASG12D in the presence or absence of pancreatitis

ABSTRACT: Bulk RNA-Seq comparing pancreatic acinar cells expressing KRASG12D in the presence or absence of pancreatitis

PROVIDER: PRJNA685442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13256800_1.fastq.gz	Fastqsanger.gz
	SRR13256800_2.fastq.gz	Fastqsanger.gz
	SRR13256801_1.fastq.gz	Fastqsanger.gz
	SRR13256801_2.fastq.gz	Fastqsanger.gz
	SRR13256802_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-Seq comparing pancreatic acinar cells expressing KRASG12D in the presence or absence of pancreatitis

Project description:ElastaseCreER-LSLKRASG12D/ROSA26YFP mice were treated or not with Cerulein to induce pancreatitis

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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

Mapping cellular plasticity through the lens of Fra1 during KrasG12D mediated pancreatic acinar to ductal metaplasia [snATAC]

Project description:Acinar cells have been proposed as a cell-of-origin for pancreatic intraepithelial neoplasia (PanIN) after undergoing a highly regulated acinar to ductal metaplasia (ADM) process. ADM can be triggered by pancreatitis causing acinar cells de-differentiate to a ductal-like state. We identify Fra1 (gene name Fosl1) as the most enriched transcription factor during KrasG12D acute pancreatitis mediated injury. We have elucidated the functional role of Fra1 by generating an acinar-specific Fosl1 knockout mouse expressing KrasG12D (Ptf1aCreERT;KrasG12D;Fosl1fl/fl;YFP) . Using single nuclei ATAC-seq and bulk-RNA seq, we used pseudotime analysis and developed a gene-regulatory network governing de-differentiation to demonstrate that Fosl1 knockout mice are delayed in the onset of ADM and accompanying recovery. Fosl1 depletion prevents the pro-inflammatory effects of G-CSF, an ADM-promoting cytokine, suggesting that the G-CSF/Fra1 signaling axis can modulate ADM. Overall, our studies mark the first time a discrete transcriptional factor has been linked to the temporal regulation of ADM.

2024-06-09 | GSE235542 | GEO

Mapping cellular plasticity through the lens of Fra1 during KrasG12D mediated pancreatic acinar to ductal metaplasia [CUT&RUN]

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Mapping cellular plasticity through the lens of Fra1 during KrasG12D mediated pancreatic acinar to ductal metaplasia [RNA-seq]

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mRNA expression pattern of KrasG12D mice with acute pancreatitis compared with wild-type mice without acute pancreatitis

2016-05-14 | GSE77983 | GEO

mRNA expression pattern of KrasG12D mice with acute pancreatitis compared with wild-type mice without acute pancreatitis

Project description:Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis. The experiment had two groups. Experiment group: KrasG12D mice with acute caerulein-induced pancreatitis (N=6). Three mice in experiment group received 1-week caerulein injection, and the other three mice received 2-week caerulein injection. All experiment group mice started to receive caerulein injection at 1-month of age, and were sacrificed at the last day of caerulein injection. Control group: wild-type mice without acute pancreatitis (N=6). The mice were sacrificed at 1.5-month of age. Whole pancreas tissue lysate samples were subjected to mRNA array assay.

2016-05-14 | E-GEOD-77983 | biostudies-arrayexpress

Bulk RNA-Seq comparing the transcriptome of pancreatic acinar cells in the presence or absence of pancreatitis

Project description:ElastaseCreER/ROSAYFP mice were treated or not with Cerulein to induce pancreatitis

2021-05-01 | GSE163254 | GEO

Bulk RNA-Seq comparing the transcriptome of pancreatic acinar cells in the presence or absence of pancreatitis

Project description:Bulk RNA-Seq comparing the transcriptome of pancreatic acinar cells in the presence or absence of pancreatitis

| PRJNA685425 | ENA

mTORC1 and mTORC2 converge on the Arp2/3 complex to promote KrasG12D-induced acinar-to-ductal metaplasia and early pancreatic carcinogenesis

Project description:Oncogenic KrasG12D, a driver mutation of pancreatic ductal adenocarcinoma (PDAC), induces neoplastic transformation of acinar cells through acinar-to-ductal metaplasia (ADM). Here, we show that both functional complexes of mTOR (mechanistic target of rapamycin kinase, mTORC1 and mTORC2) are specifically activated in ADM. Murine models uncover that mTORC1 and mTORC2 cooperate to promote KrasG12D-driven ADM development. Proteomic analyses identify Arp2/3 complex, an actin nucleator, as the common downstream effector: mTORC1 is responsible for the protein synthesis of Rac1 and Arp3 while mTORC2 promotes the Arp2/3 complex activity via Akt/Rac1 signalling. Genetic ablation of Arp2/3 complex completely arrests KrasG12D-driven ADM development. The Arp2/3 complex-mediated y-branching of actin network promotes the basolateral spread of filamentous actin, which is indispensable for acinar cells-initiated carcinogenesis. Induced by oncogenic KrasG12D, ADM is a metaplastic phenotype of acinar cells that requires extensive actin rearrangements. mTORC1 and mTORC2, downstream targets of KrasG12D, have well-established oncogenic functions in PDAC development. The actin-related protein 2/3 (Arp2/3) complex is the first identified actin nucleator. Regarded as textbook knowledge, it is activated by EGFR/Rac1 signalling to promote the polymerisation of branched actin filaments from pre-existing filaments in numerous biological contexts. Hereby, we identify that mTORC1 and mTORC2 attain a dual, yet non-redundant, regulatory role in promoting Arp2/3 complex function, which is responsible for generating basolateral filamentous actin in ADM. Thus, the role of Arp2/3 complex fills up the missing gap between putative oncogenic signals and actin dynamics underlying PDAC initiation.

2021-01-07 | PXD018296 | Pride

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