Title : PARP1-mediated PPARα poly(ADP-ribosyl)ation suppresses fatty acid oxidation in non-alcoholic fatty liver disease.

Pub. Date : 2017 May

PMID : 27979751






6 Functional Relationships(s)
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1 PARP1-mediated PPARalpha poly(ADP-ribosyl)ation suppresses fatty acid oxidation in non-alcoholic fatty liver disease. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens
2 This poly(ADP-ribosyl)ation of PPARalpha inhibits its recruitment to target gene promoters and its interaction with SIRT1, a key regulator of PPARalpha signaling, resulting in suppression of fatty acid oxidation upregulation induced by fatty acids. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens
3 This poly(ADP-ribosyl)ation of PPARalpha inhibits its recruitment to target gene promoters and its interaction with SIRT1, a key regulator of PPARalpha signaling, resulting in suppression of fatty acid oxidation upregulation induced by fatty acids. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens
4 This poly(ADP-ribosyl)ation of PPARalpha inhibits its recruitment to target gene promoters and its interaction with SIRT1, a key regulator of PPARalpha signaling, resulting in suppression of fatty acid oxidation upregulation induced by fatty acids. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens
5 This poly(ADP-ribosyl)ation of PPARalpha inhibits its recruitment to target gene promoters and its interaction with SIRT1, a key regulator of PPARalpha signaling, resulting in suppression of fatty acid oxidation upregulation induced by fatty acids. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens
6 CONCLUSIONS: Our data indicate that PARP1 is activated in fatty liver, which prevents maximal activation of fatty acid oxidation by suppressing PPARalpha signaling. Fatty Acids peroxisome proliferator activated receptor alpha Homo sapiens