Figure 2
Figure 2. Lack of TβRII expression is responsible for the TGF-β signaling defect in PEL. (A) Levels of TGF-β pathway components compared among PEL cells (BC1, BC3, BC5, BCBL-1) and other B-cell lymphoma cell lines (Ramos, BJAB, Namalwa, BCKN1) that express relatively normal levels of these components. (B) TβRII expression measured by real-time PCR. (C) TGF-β-responsive reporter activity on transfection of TβRII. (D) RT-PCR analysis of TβRII expression in BC3 cells transduced with pHR-Sin-CSGW-TβRII. (E) TGF-β–driven reporter activity and (F) Smad2 phosphorylation in TβRII-transduced BC3 cells. Error bars represent SD.

Lack of TβRII expression is responsible for the TGF-β signaling defect in PEL. (A) Levels of TGF-β pathway components compared among PEL cells (BC1, BC3, BC5, BCBL-1) and other B-cell lymphoma cell lines (Ramos, BJAB, Namalwa, BCKN1) that express relatively normal levels of these components. (B) TβRII expression measured by real-time PCR. (C) TGF-β-responsive reporter activity on transfection of TβRII. (D) RT-PCR analysis of TβRII expression in BC3 cells transduced with pHR-Sin-CSGW-TβRII. (E) TGF-β–driven reporter activity and (F) Smad2 phosphorylation in TβRII-transduced BC3 cells. Error bars represent SD.

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