Ectopic expression of H2AX protein promotes TrkA-induced cell death via modulation of TrkA tyrosine-490 phosphorylation and JNK activity upon DNA damage

► We established TrkA-inducible U2OS cells stably expressing GFP-H2AX proteins. ► GFP-H2AX was colocalized with TrkA in the cytoplasm. ► γH2AX production was significantly increased upon activation of TrkA and suppressed by TrkA inhibitor or JNK inhibitor. ► Ectopic expression of H2AX promoted TrkA-mediated cell death through the modulation of TrkA tyrosine-490 phosphorylation and JNK activity upon DNA damage.