https://map4k-receptor.com/ind....ex.php/outcome-of-re
CB2 phrase had been closely correlated using the progression of renal fibrosis and followed by the activation of β-catenin. Moreover, CB2 caused the forming of a β-arrestin 1/Src/β-catenin complex, which more triggered the nuclear translocation of β-catenin and caused fibrotic injury. Incubation with XL-001, an inverse agonist to CB2, or knockdown of β-arrestin 1 inhibited CB2-triggered activation of β-catenin and fibrotic damage. Notably, CB2 potentiated