<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE137320" accession="SRP221455">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP221455</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA565167</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE137320</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [CUT&amp;RUN]</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>The transcription factor c-Maf is an essential regulator of group 3 ILC homeostasis and effector plasticity. c-Maf limits acquisition of the type 1 program and conversion to the ILC1 fate through restraint of T-bet expression and function. Overall design: Evaluation of differential H3K27ac and H3K27me3 histone marks in cohoused Maf-deficient NKp46+ ILC3. The CUT&amp;RUN  protocol was performed on replicate samples of  NKp46+ ILC3  isolated from the small intestine lamina propria of Maf+/+ Il7r-Cre and Maf fl/fl Il7r-Cre mice.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE137320</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>31570496</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA565163</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
