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

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 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 in NF-κB regulation in response to DNA damage. Here we demonstrate for the first time that regulates NF-κB upstream signaling by activating the IκB kinase (IKK) and the degradation of IκB. Furthermore, 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 duanyu1531η confers protection against DNA damage-induced apoptosis. Our present study suggests that duanyu1531η is involved in NF-κB signaling leading to drug resistance.

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