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Three HepG2 cell models were constructed to demonstrate that inhibition of CD36 palmitoylation could simultaneously activate the AMPK pathway to improve lipid metabolism and inhibit the JNK pathway to reduce inflammation (205)

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Several charged residues from HGF I-K1, including His158, Glu159, Arg181, Glu195, Arg197, and Arg554, participate in this interaction

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