<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE168331" accession="SRP309457">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP309457</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA706939</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE168331</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Genome-wide H3K56ac profiling after Sirt6 knockdown in mESCs [ChIP-seq]</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>Sirt6, the NAD+-dependent deacetylase, has been described to deacetylate H3K9, H3K18, and H3K56. However, analysis of the acetylation status revealed that loss of Sirt6 caused a massive increase of histone H3K56ac levels but no detectable change of histone H3K9ac and H3K18ac, indicating that SIRT6 is the dominant deacetylase for H3K56ac in muscle stem cells (MuSCs). Further, we investigate genome-wide H3K56ac profiling in the absence of Sirt6 in MuSCs and mouse embryonic stem cells (mESCs) using high throughput sequencing (ChIP-seq). Overall design: ChIP-seq experiment to determine genome-wide H3K56ac distribution in scrabled control and Sirt6 knockdown mouse embryonic stem cells</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE168331</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA706934</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
