<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY accession="ERP118222" alias="ena-STUDY-Charite Universitaetsmedizin-04-11-2019-11:09:18:379-16" center_name="Charite Universitaetsmedizin">
    <IDENTIFIERS>
      <PRIMARY_ID>ERP118222</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject">PRJEB35204</EXTERNAL_ID>
      <SUBMITTER_ID namespace="Charite Universitaetsmedizin">ena-STUDY-Charite Universitaetsmedizin-04-11-2019-11:09:18:379-16</SUBMITTER_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Transcriptome analysis of murine Hdac2 knockout pancreatic tumor cells.</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>We performed a knockout of Hdac2 in a dual recombinase system based and KrasG12D/+ driven mouse model of pancreatic ductal adenocarcinoma (n=3 biological; n= 2 technical replicates).Tamoxifen (4-OHT) treatment for 8 days excised the floxed Hdac2 alleles by the CreERT2 fusion protein. Ethanol (EtOH) served as a vehicle control. Genotype: FSF-KrasG12D/+, FSF-Trp53del/+, Pdx1-Flp, R26CAG-FSF-CreERT2/+, Pdk1loxP/+, Hdac2loxP/loxP</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>HDAC in PDAC</CENTER_PROJECT_NAME>
      <STUDY_DESCRIPTION>We performed a knockout of Hdac2 in a dual recombinase system based and KrasG12D/+ driven mouse model of pancreatic ductal adenocarcinoma (n=3 biological; n= 2 technical replicates).Tamoxifen (4-OHT) treatment for 8 days excised the floxed Hdac2 alleles by the CreERT2 fusion protein. Ethanol (EtOH) served as a vehicle control. Genotype: FSF-KrasG12D/+, FSF-Trp53del/+, Pdx1-Flp, R26CAG-FSF-CreERT2/+, Pdk1loxP/+, Hdac2loxP/loxP</STUDY_DESCRIPTION>
    </DESCRIPTOR>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>ENA-FIRST-PUBLIC</TAG>
        <VALUE>2020-02-19</VALUE>
      </STUDY_ATTRIBUTE>
      <STUDY_ATTRIBUTE>
        <TAG>ENA-LAST-UPDATE</TAG>
        <VALUE>2021-09-01</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
