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Atypical PKCs, NF-κB, and Inflammation

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Protein Kinase C in Cancer Signaling and Therapy

Part of the book series: Current Cancer Research ((CUCR))

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Abstract

Complex biological processes, such as inflammation and cancer, rely on the crosstalk and activation of distinct cellular networks that control gene expression. Central to this process is the transcription factor NF-κB. In this chapter, we focus on the role of the atypical protein kinase C (PKC) isoforms (aPKC) in inflammation and cancer through the activation of this transcription factor in vivo. The aPKCs are key members of a network of kinases, adapters and regulators, such as p62 and Par-4, which confer functional plasticity and specificity to this critical pathway. Here, we summarize the molecular mechanisms that govern that network, learnt from the knock-out mouse models, to unravel its role and function in vivo.

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Diaz-Meco, M.T., Moscat, J. (2010). Atypical PKCs, NF-κB, and Inflammation. In: Kazanietz, M. (eds) Protein Kinase C in Cancer Signaling and Therapy. Current Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-543-9_10

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