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        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">lipidosis (course)</rdfs:label>
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        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">PPARalpha inactivation [alcoholic fatty liver]</rdfs:label>
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        <ns3:IAO_0000115 rdf:datatype="http://www.w3.org/2001/XMLSchema#string">PPARalpha inactivation is a subtype of inactivation: A process that changes the activity of the activating PPAR alpha (Peroxisome Proliferator Activated Receptor Alpha) with a nuclear receptor role to be lower.
This entity is a specific course-dependent process. This process can constitute the course of alcoholic fatty liver.</ns3:IAO_0000115>
        <ns3:IAO_0000232 rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Reactome

The set of genes regulated by PPAR-alpha is not fully known in humans, however many examples have been found in mice. Genes directly activated by PPAR-alpha contain peroxisome proliferator receptor elements (PPREs) in their promoters and include:
1) genes involved in fatty acid oxidation and ketogenesis (Acox1, Cyp4a, Acadm, Hmgcs2);
2) genes involved in fatty acid transport (Cd36, , Slc27a1, Fabp1, Cpt1a, Cpt2);
3) genes involved in producing fatty acids and very low density lipoproteins (Me1, Scd1);
4) genes encoding apolipoproteins (Apoa1, Apoa2, Apoa5);
5) genes involved in triglyceride clearance ( Angptl4);
6) genes involved in glycerol metabolism (Gpd1 in mouse);</ns3:IAO_0000232>
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