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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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PKC-beta controls I kappa B kinase lipid raft recruitment and activation in response to BCR signaling.

NF-kappa B signaling is required for the maintenance of normal B lymphocytes, whereas dysregulated NF-kappa B activation contributes to B cell lymphomas. The events that regulate NF-kappa B signaling in B lymphocytes are poorly defined. Here, we demonstrate that PKC-beta is specifically required for B cell receptor (BCR)-mediated NF-kappa B activation. B cells from protein kinase C-beta (PKC-beta)-deficient mice failed to recruit the I kappa B kinase (IKK) complex into lipid rafts, activate IKK, degrade I kappa B or up-regulate NF-kappa B-dependent survival signals. Inhibition of PKC-beta promoted cell death in B lymphomas characterized by exaggerated NF-kappa B 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.[1]

References

  1. PKC-beta controls I kappa B kinase lipid raft recruitment and activation in response to BCR signaling. Su, T.T., Guo, B., Kawakami, Y., Sommer, K., Chae, K., Humphries, L.A., Kato, R.M., Kang, S., Patrone, L., Wall, R., Teitell, M., Leitges, M., Kawakami, T., Rawlings, D.J. Nat. Immunol. (2002) [Pubmed]
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