Fig. 5.
Fig. 5. Modulation of NF-κB activation by IGtranslocations. / Genes involved in these processes, which are deregulated by IGtranslocations, are shown in yellow. NF-κB activation by extracellular signals such as TNF is mediated via a signaling pathway involving the death initiator signaling complex (DISC), TRAF2, NIK, IKK, and phosphorylation and degradation of IκB. NF-κB2:Truncated NF-κB2 proteins as found in some lymphomas are constitutively active transcription factors, mediating up-regulation of NF-κB target genes, including those involved in proliferation and apoptosis, such as cyclin D1 and Bcl-xL. BCL10:BCL10 mediates both NF-κB activation, through its recruitment to the DISC, and apoptosis via mechanisms that remain unclear. Truncated BCL10 maintains its NF-κB–activating functions but loses its apoptotic activity. BCL3: BCL3 is an IκB family member, which mediates transcriptional up-regulation of NF-κB target genes through interaction with p50/p52 homodimers.

Modulation of NF-κB activation by IGtranslocations.

Genes involved in these processes, which are deregulated by IGtranslocations, are shown in yellow. NF-κB activation by extracellular signals such as TNF is mediated via a signaling pathway involving the death initiator signaling complex (DISC), TRAF2, NIK, IKK, and phosphorylation and degradation of IκB. NF-κB2:Truncated NF-κB2 proteins as found in some lymphomas are constitutively active transcription factors, mediating up-regulation of NF-κB target genes, including those involved in proliferation and apoptosis, such as cyclin D1 and Bcl-xL. BCL10:BCL10 mediates both NF-κB activation, through its recruitment to the DISC, and apoptosis via mechanisms that remain unclear. Truncated BCL10 maintains its NF-κB–activating functions but loses its apoptotic activity. BCL3: BCL3 is an IκB family member, which mediates transcriptional up-regulation of NF-κB target genes through interaction with p50/p52 homodimers.

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