例如:"lncRNA", "apoptosis", "WRKY"

Expression of the epidermodysplasia verruciformis-associated genes EVER1 and EVER2 is activated by exogenous DNA and inhibited by LMP1 oncoprotein from Epstein-Barr virus.

J. Virol.2015 Jan 15;89(2):1461-7. Epub 2014 Nov 05
Cecilia Frecha 1 , Sébastien A Chevalier 1 , Patrick van Uden 1 , Ivonne Rubio 1 , Maha Siouda 1 , Djamel Saidj 1 , Camille Cohen 2 , Patrick Lomonte 2 , Rosita Accardi 1 , Massimo Tommasino 3
Cecilia Frecha 1 , Sébastien A Chevalier 1 , Patrick van Uden 1 , Ivonne Rubio 1 , Maha Siouda 1 , Djamel Saidj 1 , Camille Cohen 2 , Patrick Lomonte 2 , Rosita Accardi 1 , Massimo Tommasino 3
+ et al

[No authors listed]

Author information
  • 1 Section of Infections, Infections and Cancer Biology Group, International Agency for Research on Cancer, Lyon, France.
  • 2 Virus & Centromère Team, Centre de Génétique et Physiologie Moléculaire et Cellulaire, CNRS, UMR5534, Lyon, France Université de Lyon 1, Lyon, France Laboratoire d'Excellence, LabEX DEVweCAN, Lyon, France.
  • 3 Section of Infections, Infections and Cancer Biology Group, International Agency for Research on Cancer, Lyon, France tommasino@iarc.fr.

摘要


EVER1 and EVER2 are mutated in epidermodysplasia verruciformis patients, who are susceptible to human betapapillomavirus (HPV) infection. It is unknown whether their products control the infection of other viruses. Here, we show that the expression of both genes in B cells is activated immediately after Epstein-Barr virus (EBV) infection, whereas at later stages, it is strongly repressed via activation of the NF-κB signaling pathway by latent membrane protein 1 (LMP1). Ectopic expression of EVER1 impairs the ability of EBV to infect B cells.