Figure 5
Figure 5. MYD88 is a regulator of BTK activity in L265P-expressing WM cells. (A) Phospho-BTK and total BTK levels following the knockdown of MYD88 in L265P-expressing WM cells. The relative density of phosphorylated vs total BTK was analyzed by densitometry measurements and normalized to the values of control vectors. (B) Phospho-BTK and total BTK levels were examined after the use of inhibitors of IRAK 1 and 4 or MYD88 by western blot. (C) Phospho-IRAK1 and total IRAK1 levels following ibrutinib treatment of BCWM.1 and MWCL-1 cells. (D) Phospho-BTK levels following use of an MYD88 inhibitor (100 μM) by phospho-flow cytometric analysis in BCWM.1, MWCL-1, OCI-Ly3, OCI-Ly19, and Ramos cells. (E) Phosphorylated BTK and BTK levels as determined by western blot analysis following the knockdown of IRAK 1, and IRAK 4 in BCWM.1 cells.

MYD88 is a regulator of BTK activity in L265P-expressing WM cells. (A) Phospho-BTK and total BTK levels following the knockdown of MYD88 in L265P-expressing WM cells. The relative density of phosphorylated vs total BTK was analyzed by densitometry measurements and normalized to the values of control vectors. (B) Phospho-BTK and total BTK levels were examined after the use of inhibitors of IRAK 1 and 4 or MYD88 by western blot. (C) Phospho-IRAK1 and total IRAK1 levels following ibrutinib treatment of BCWM.1 and MWCL-1 cells. (D) Phospho-BTK levels following use of an MYD88 inhibitor (100 μM) by phospho-flow cytometric analysis in BCWM.1, MWCL-1, OCI-Ly3, OCI-Ly19, and Ramos cells. (E) Phosphorylated BTK and BTK levels as determined by western blot analysis following the knockdown of IRAK 1, and IRAK 4 in BCWM.1 cells.

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