<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE164025" accession="SRP299767">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP299767</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA688636</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE164025</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Astrocytes Tet1 regulates neuronal  development and cognition through  modulating GluA1</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Using RNA sequencing, we found that Tet1 alters gene expression. Mechanistically, we found that Tet1 deficiency leads to the abnormal Ca2+ signaling by regulating the expression of GluA1, which can be rescued by ectectopic expression of GluA1. Collectively, our findings suggest that Tet1 plays important functions by regulating astrocytes Ca2+ signaling. Overall design: Astrocytes were isolated from two P1 Tet1 WT or KO mice and cultured in a PDL-coated T25 flask for about 7 days.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE164025</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>34778243</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
