Fig. 4: Activated SYK promotes STAT3 and AKT signaling as an intermediary of mutated MYD88.
From: SYK is activated by mutated MYD88 and drives pro-survival signaling in MYD88 driven B-cell lymphomas
Impact of SYK knockdown by lentiviral transduction (a) or use of SYK inhibitors tamatinib (TAM) or entospletinib (ENTO) (b) on p-STAT3 (Y705), p-ATK (S473), p-BTK (Y223), p-IRAK1(T209), and p-IRAK4(T345/S346) in MYD88-mutated BCWM.1 WM and MYD88/CD79B mutated TMD8 ABC DLBCL cells. The results from experiments assessing the impact of mutated (L265P) or wild-type MYD88 expression on p-SYK (pY525-pY526), p-STAT3 (pY705), and p-AKT (pS473) in the presence or absence of SYK inhibitors (c). GAPDH was used to depict uniform protein loading. Studies were performed twice, and representative experimental set is shown.
