<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE122834" accession="SRP170067">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP170067</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA506452</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE122834</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Roles of HDAC1 and HDAC2 in the developing mouse brain</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>In this study, we investigated the role of HDAC1 and HDAC2 in the developing mouse brain. We found that the removal of HDAC1 and HDAC2 caused severe malformation. To examine the molecular mechanisms underlying the cortical malformation, we examined the transcriptome in both WT and HDAC1/2 deficient brains. We found that many genes that are associated with transcription were misregulated in HDAC1 and HDAC2 mutant brains. This result provides a resource for studying gene expression controlled by HDAC1 and HDAC2. Overall design: Mouse embryonic for brains were isolated from E12.5 embryos. Total RNAs were extracted using Trizol reagent and applied for RNA sequencing subsequently.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE122834</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>30709655</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
