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GPR35 agonists (YE120, zaprinast, and pamoic acid) promoted wound repair in the focus-dependent manner independently of mobile proliferation, While a selected GPR35 antagonist CID2745687, forskolin, and pertussis toxin reversed the YE120-induced impact. YE120 amplified the mRNA expression of fibronectin and its receptor integrin αfive, and ERK1/tw