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in a 503A licensed compounding facility
(1999) discovered in 1999 that DFO might lessen APAP-induced liver damage by intracellular chelating iron
doi: 10.3389/fcimb.2018.00013
This interaction was mapped at the hydrophobic domain of G0S2 and the patatin-like domain of PNPLA2, whereby overexpression of G0S2 diminished adipocyte lipolysis, and deletion increased both basal and stimulated lipolysis (52)
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