<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE126047" accession="SRP183465">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP183465</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA520870</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE126047</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Small RNA profiling in mouse alcohol-induced liver injury and steatosis model.</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Transcriptome Analysis"/>
      <STUDY_ABSTRACT>Complement is known to play a role in alcoholic fatty liver disease (AFLD), but the underlying mechanisms are poorly understood, thereby constraining the development of a rational approach for therapeutic intervention in the complement system.here we demonstrate protection in wild type mice by treatment with CR2-Crry, a C3 inhibitor that specifically targets sites of complement activation. We found that the expression of glycine transfer (t) RNA-derived fragments (Gly-tRFs) is upregulated in ethanol-fed mice, and that inhibition of Gly-tRFs in vivo decreases chronic ethanol-feeding-induced hepatosteatosis without affecting inflammation Overall design: small RNAs expression profiling of liver tissues obtained after 16 days EtOH feed.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE126047</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>31076642</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
  </STUDY>
</STUDY_SET>
