Journal
CANCER CELL
Volume 5, Issue 4, Pages 353-364Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(04)00084-4
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Funding
- NCI NIH HHS [P50-CA-93683-02] Funding Source: Medline
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NPM-ALK characterizes anaplastic large cell lymphoma (ALCL), as does the high expression of CD30, a feature shared with H-RS cells of classic Hodgkin's lymphoma. In H-RS cells, ligand-independent signaling by overexpressed CD30 drives constitutive NF-B-K activation, which is absent in ALCL cells. Here we show that NPM-ALK impedes CD30 signaling and NF-B-K activation, dependent on both ALK kinase activity and the N-terminal NPM domain. NPM-ALK transduction into H-RS cell lines abrogates recruitment and aggregation of TRAF proteins, inducing an ALCL-like morphology and phenotype. TRAF2 associates with NPM-ALK at a consensus binding motif located in the kinase domain. Thus, NPM-ALK abrogates CD30-driven NF-B-K activation and can also induce an ALCL phenotype, distinguishing ALCL cells from H-RS cells of T cell origin.
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