Figure 3.
Figure 3. Deregulation of BCL6 activity by multiple mechanisms in DLBCL. Recurrent genetic alterations deregulating the function of BCL6 in DLBCL, either directly (by targeting the BCL6 gene) or indirectly (by targeting modulators of its activity). Only representative biological programs suppressed by BCL6 in the GC and disrupted as a consequence of these lesions are shown. Symbols depict loss-of-function (crosses) and gain-of-function (lightning bolt) genetic alterations. Asterisk represents point mutations in the BCL6 regulatory sequences, abrogating DNA binding sites used by the IRF4 transcription factor or by the BCL6 protein itself to negatively regulate BCL6 transcription. Reprinted from Pasqualucci and Dalla-Favera135 with permission.

Deregulation of BCL6 activity by multiple mechanisms in DLBCL. Recurrent genetic alterations deregulating the function of BCL6 in DLBCL, either directly (by targeting the BCL6 gene) or indirectly (by targeting modulators of its activity). Only representative biological programs suppressed by BCL6 in the GC and disrupted as a consequence of these lesions are shown. Symbols depict loss-of-function (crosses) and gain-of-function (lightning bolt) genetic alterations. Asterisk represents point mutations in the BCL6 regulatory sequences, abrogating DNA binding sites used by the IRF4 transcription factor or by the BCL6 protein itself to negatively regulate BCL6 transcription. Reprinted from Pasqualucci and Dalla-Favera135  with permission.

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