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. Author manuscript; available in PMC: 2016 Nov 1.

Published in final edited form as: Free Radic Biol Med. 2015 May 21;88(0 0):158–167. doi: 10.1016/j.freeradbiomed.2015.05.017

Notch-Nrf2 axis. (A) Possible links for biological events occurring in postnatal tissues through this axis. (B) Scheme for hijacking of the NOTCH-NRF2 axis in humans by viral infections such as EBV or KSHV, thereby facilitating oncogenesis. Infected cells express EBNA2 or RTA, which are viral genome products exhibiting NICD mimicry structures for association with Rbpjκ. This mimicry enhances expression of NOTCH target genes such as cMYC, BCL2 and possibly NRF2. In the case of KSHV, RTA can recruit cellular RBPJκ onto its gene promoters for expression of viral genes such as vFLIP, vIL6 and vGPCR. These viral and abused cellular gene products together might contribute to oncogenesis. NRF2 signaling consequently supports the survival of the virus infected cell.

Notch-Nrf2 axis. (A) Possible links for biological events occurring in postnatal tissues through this axis. (B) Scheme for hijacking of the NOTCH-NRF2 axis in humans by viral infections such as EBV or KSHV, thereby facilitating oncogenesis. Infected cells express EBNA2 or RTA, which are viral genome products exhibiting NICD mimicry structures for association with Rbpjκ. This mimicry enhances expression of NOTCH target genes such as cMYC, BCL2 and possibly NRF2. In the case of KSHV, RTA can recruit cellular RBPJκ onto its gene promoters for expression of viral genes such as vFLIP, vIL6 and vGPCR. These viral and abused cellular gene products together might contribute to oncogenesis. NRF2 signaling consequently supports the survival of the virus infected cell.