HSP90 inhibition attenuates activated BCR signaling. (A-B) Immunoblots of CCL from DG75 (left) and Daudi (right) cells that were treated with DMSO, AT13387, STA-9090, or PRT062607 for indicated durations, using antibodies against (p)AKT (A) and (p) extracellular signal-regulated kinase (pERK) (B). Actin was used as loading control. (C) DG75 and Daudi cells were treated as in panels A-B, subsequently loaded with the ratiometric Ca²⁺ chelator INDO‐1‐AM, and subjected to Ca²⁺ flux analysis by flow cytometry. BCR engagement was induced after 30 seconds using 5 µg/mL goat-anti-human immunoglobulin M. (D) Cell viability of the ABC-DLBCL cell lines TMD8 and Ly10 treated with the indicated concentrations of AT13387 and STA-9090 for 24 hours. Values were determined by a 3-(4,5 dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl-2-(4-sulfophenyl)-2H-tetrazolium assay and normalized to DMSO controls.