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. 2008 Dec 8;105(50):19643–19648. doi: 10.1073/pnas.0810965105

Fig. 1.

Fig. 1.

Tcl1 activates NF-κB-dependent transcription. (A) Chromatograms of sequences surrounding T38I, E40D, R52H mutations obtained from sequencing of buccal swab constitutional DNA, B-CLL DNA, and results of RT-PCR (for T38I mutant) using RNA from B-CLL cells. (B) Tcl1 activates NF-κB. NIH 3T3 cells were cotransfected with 50 ng of pNF-kB-Luc reporter and 50 ng of pRL-TK Renilla reporter constructs. In addition, 1.5 μg of CMV5-empty vector, or a combination of 0.75 μg of CMV5-empty vector and 0.75 μg of CMV5-Tcl1 WT, or CMV5-Tcl1 T38I constructs were used. Five nanograms of pFC-MEKK was added where indicated. Cells were treated with 200 nmol/L of Wortmannin overnight, where indicated. The normalized promoter activity of pNF-kB-Luc in NIH 3T3 cells transfected with CMV5-empty vector was set as 1. (C) Tcl1 interacts with p300. (Upper) Some 293 cells were cotransfected with p300-HA and Omni-Fhit or p300-HA and Omni-Tcl1 constructs. After lysis, immunoprecipitations were carried out with anti-HA, IgG, or anti-omni antibodies. Western blot analysis was carried out as indicated. (Lower) Daudi cells were lysed and immunoprecipitations were carried out with anti-Tcl1 antibody, IgG, or anti-p300 antibody. Unlabeled higher band in the Tcl1 panel represents IgG. Western blot analysis was carried out as indicated.