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Genome-wide map of Gata6 DNA binding in mouse pancreas

ABSTRACT: We have previously described in mouse models that pancreas-specific deletion of Gata6 results in pancreas alterations by rendering pancreatic acinar cells in a non-fully differentiation state, and furthermore it accelerates tumor initiation and progression in a pro-tumorigenic context (KrasG12V expression). We aim to determine the sites where Gata6 binds at the genome-wide level in the pancreas to unveil why its loss leads to altered pancreatic function and enhanced tumor formation when coexpressed with KrasG12V. Gata6 ChIP-Seq in the mouse pancreas

ORGANISM(S): Mus musculus

SUBMITTER: Francesc Madriles

PROVIDER: E-GEOD-57090 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The acinar regulator Gata6 suppresses KrasG12V-driven pancreatic tumorigenesis in mice.

Martinelli Paola P Madriles Francesc F Cañamero Marta M Pau Enrique Carrillo-de Santa EC Pozo Natalia Del ND Guerra Carmen C Real Francisco X FX

Gut 20150116 3

<h4>Background and aims</h4>Gata6 is required to complete and maintain acinar differentiation in the mouse pancreas. Pancreas-specific Gata6 ablation during development causes extensive and persistent acinar-ductal metaplasia, which is considered an initial step of mutant KRas-driven carcinogenesis. Therefore, the Gata6-null pancreas might represent a tumour-prone environment. We investigated whether Gata6 plays a role during pancreatic tumorigenesis.<h4>Design</h4>We analysed genetically engine ...[more]

PMID: 25596178

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