<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE106679" accession="SRP124619">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP124619</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA417668</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE106679</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Brain-specific deletion of histone variant H2A.z results in cortical neurogenesis defects and neurodevelopmental disorder</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>ChIP experiment was performed with antibody against H3K36me3 (active motif; 61101). we generated genome-wide characterization of H3K36me3 occupancy in E13 H2A.Z cKO forebrain. We found H3K36me3 is decreased throughout the whole genome in E13 H2A.Z cKO forebrain. Overall design: Genomic characterization of H3K36me3 binding in E13 WT and brain-specific deficit H2A.z forebrain.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE106679</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
