1. Academic Validation
  2. Protein kinase Cη activates NF-κB in response to camptothecin-induced DNA damage

Protein kinase Cη activates NF-κB in response to camptothecin-induced DNA damage

  • Biochem Biophys Res Commun. 2011 Aug 26;412(2):313-7. doi: 10.1016/j.bbrc.2011.07.090.
Hadas Raveh-Amit 1 Naama Hai Noa Rotem-Dai Galit Shahaf Jacob Gopas Etta Livneh
Affiliations

Affiliation

  • 1 The Shraga Segal Department of Microbiology and Immunology, Faculty of Health Sciences, The Cancer Research Center, Ben-Gurion University of the Negev, Israel.
Abstract

The nuclear factor κB (NF-κB) family of transcription factors participates in the regulation of genes involved in innate- and adaptive-immune responses, cell death and inflammation. The involvement of the Protein kinase C (PKC) family in the regulation of NF-κB in inflammation and immune-related signaling has been extensively studied. However, not much is known on the role of PKC in NF-κB regulation in response to DNA damage. Here we demonstrate for the first time that PKC-eta (PKCη) regulates NF-κB upstream signaling by activating the IκB kinase (IKK) and the degradation of IκB. Furthermore, PKCη enhances the nuclear translocation and transactivation of NF-κB under non-stressed conditions and in response to the Anticancer drug camptothecin. We and Others have previously shown that PKCη confers protection against DNA damage-induced Apoptosis. Our present study suggests that PKCη is involved in NF-κB signaling leading to drug resistance.

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