Figure 5.
Pharmacologic inhibition of the validated hits in MM patient samples upregulate cell surface BCMA levels. Bone marrow–mononuclear cells isolated from bone marrow aspirates from various patients with MM were treated with indicated concentration of a class II HDAC inhibitor (TMP269), a γ-secretase inhibitor (RO4929097), and a Sec61 inhibitor (PS3061) for 24 hours. Cells were stained for cell surface CD138, BCMA, and CD38 and analyzed by using flow cytometry. Fold change in BCMA and CD38 levels were determined in CD138+ live cell populations. Data are means of 3 technical replicates, and error bars denote standard deviations.

Pharmacologic inhibition of the validated hits in MM patient samples upregulate cell surface BCMA levels. Bone marrow–mononuclear cells isolated from bone marrow aspirates from various patients with MM were treated with indicated concentration of a class II HDAC inhibitor (TMP269), a γ-secretase inhibitor (RO4929097), and a Sec61 inhibitor (PS3061) for 24 hours. Cells were stained for cell surface CD138, BCMA, and CD38 and analyzed by using flow cytometry. Fold change in BCMA and CD38 levels were determined in CD138+ live cell populations. Data are means of 3 technical replicates, and error bars denote standard deviations.

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