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

Hadas Raveh-Amit, Naama Hai, Noa Rotem-Dai, Galit Shahaf, Jacob Gopas, Etta Livneh

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

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.

Original languageEnglish
Pages (from-to)313-317
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume412
Issue number2
DOIs
StatePublished - 26 Aug 2011

Keywords

  • Camptothecin
  • DNA damage
  • Nuclear factor κB transactivation
  • Protein kinase C
  • RelA/P65

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