NF-κB signaling has a pivotal role in innate immunity with uncontrolled NF-κB activation contributing to B cell lymphoma development. However, the mechanisms that regulate NF-κB signaling in B-lymphocytes have been poorly understood. In 15 July advanced online Nature Immunology, Thomas Su and colleagues from University of California, Los Angeles, shows that protein kinase C-β (PKC-β) controls IκB kinase lipid raft recruitment and is specifically required for B cell receptor–mediated NF-κB activation (Nat Immunol 2002 DOI:10.1038/ni823).

Su et al. worked with B cells from PKC-β–deficient mice and observed that these cells failed to recruit the IκB kinase (IKK) complex into lipid rafts, activate IKK, degrade IκB or up-regulate NF-κB–dependent survival signals and subsequently died. In addition, inhibition of PKC-β promoted cell death in B lymphomas characterized by exaggerated NF-κB activity.

"Our data suggest that a combination of standard chemotherapy with drugs targeting the PKC-βκ–dependent NF-κκB survival pathway may...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!
Already a member?