Journal
NATURE IMMUNOLOGY
Volume 3, Issue 8, Pages 780-786Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni823
Keywords
-
Categories
Funding
- NCI NIH HHS [CA09120, CA74929, CA81140] Funding Source: Medline
- NIAID NIH HHS [AI38348, AI33617] Funding Source: Medline
- NICHD NIH HHS [HD37091] Funding Source: Medline
- NIGMS NIH HHS [GM08042] Funding Source: Medline
Ask authors/readers for more resources
NF-kappaB signaling is required for the maintenance of normal B lymphocytes, whereas dysregulated NF-kappaB activation contributes to B cell lymphomas. The events that regulate NF-kappaB signaling in B lymphocytes are poorly defined. Here, we demonstrate that PKC-beta is specifically required for B cell receptor (BCR)-mediated NF-kappaB activation. B cells from protein kinase C-beta (PKC-beta)-deficient mice failed to recruit the IkappaB kinase (IKK) complex into lipid rafts, activate IKK, degrade IkappaB or up-regulate NF-kappaB-dependent survival signals. Inhibition of PKC-beta promoted cell death in B lymphomas characterized by exaggerated NF-kappaB activity. Together, these data define an essential role for PKC-beta in BCR survival signaling and highlight PKC-beta as a key therapeutic target for B-lineage malignancies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available