<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE125264" accession="SRP179993">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP179993</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA515709</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE125264</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Global gene expression profile of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Febrile temperature enhanced Th17 differentiation in Smad4 SUMOylation-dependent manner. Smad4-deficiency impaired the febrile temperature-enhanced Th17 differentiation. In order to understand how febrile temperature and Smad4 contribute to Th17 pathogenicity, we conducted transcriptional analysis of wild type and Smad4-deficient Th17 cells cultured at 37°C and 39.5°C (Day 3). Overall design: Naive CD4+ T cells were sorted from wild type and Smad4-deficient mice and differentiated into Th17 cells at 37°C and 39.5°C. The total RNA was extracted with Trizol (Life Technologies) according to manufacturer's instructions, and the RNA-seq library was constructed with NEXTflex RNA-seq kit (Bioo Scientific) and sequenced with BGI500 platform by BGI Genomics and successfully mapped to mouse genome. Reads counts were normalized based on RPKM/FPKM, fold changes were calculated for all possible comparisons.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE125264</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>32049050</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA515712</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
