Fig. 3.

Atiprimod inhibits the phosphorylation of STAT3, STAT5, and AKT in FDCP-EpoR cells expressing mutant JAK2^V617F FDCP-EpoR cell lines carrying JAK2^WT or JAK2^V617F were treated with equipotent doses (IC₂₀, IC₅₀, and IC₈₀) of atiprimod for 24 h. Extracted cell lysates were separated on a 4–12% SDS-PAGE gel, and western blotting was performed using mouse monoclonal antibodies against the specified proteins. After stripping, membranes were reprobed with rabbit anti-total STAT3, STAT5 and AKT. β-actin served as loading control