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GPR35 agonists (YE120, zaprinast, and pamoic acid) promoted wound mend within a focus-dependent manner independently of cell proliferation, whereas a selected GPR35 antagonist CID2745687, forskolin, and pertussis toxin reversed the YE120-induced outcome. YE120 amplified the mRNA expression of fibronectin and its receptor integrin ?five, and ERK1/tw

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