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Determining the Destiny of NF- B after TCR Ligation: It’s CARMA1

Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA

SUMMARY

In T lymphocytes, the "novel" protein kinase C (PKC ) isoform and the transcription factor nuclear factor-B (NF-B) are required for cell proliferation and the production of cytokines in response to T cell activation; however, the molecular interactions that link PKC and NF-B have remained unknown. Two recent reports demonstrate that CARMA1 (caspase recruitment domain-containing membrane-associated guanylate kinase protein-1) bridges the gap between PKC and the IB kinase (IKK)-dependent activation of NF-B in T cells. Excessive T lymphocyte activation and proliferation are hallmarks of T cell-derived leukemias. Given that CARMA1 is specifically expressed in lymphoid tissues, could pharmacological inhibitors be designed to inhibit CARMA1’s (or PKC’s) ability to promote the activation of NF-B?

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				P. N. Moynagh The NF-{kappa}B pathway J. Cell Sci., October 15, 2005; 118(20): 4589 - 4592. [Full Text] [PDF]