Fig. 1
From: UBXN3B positively regulates STING-mediated antiviral immune responses

UBXN3B is critical for IFN-I induction by and control of HSV-1 infection in vivo. a Immunoblots showing Ubxn3b knockout efficiency in various tissues without/with tamoxifen (TMX) treatment in Cre+/− Ubxn3bflox/flox mice. Tubulin is a housekeeping protein control. b, c The survival curves of tamoxifen (TMX)-treated Ubxn3bflox/flox, TMX-treated Cre+/−, mock-treated Cre+/− Ubxn3bflox/flox (designated Ubxn3b+/+) and TMX-treated Cre+/− Ubxn3bflox/flox (designated Ubxn3b−/−) littermate and Sting−/− mice challenged with 1 × 107 plaque-forming units (PFU) per mouse of HSV-1 i.v. N = 8–9 mice/genotype. ***P < 0.001 (log-rank test). d The serum IFN-I concentrations (mean ± s.e.m) of mice challenged with 2 × 106 PFU per mouse of HSV-1 i.v. **P < 0.01; *P < 0.05 (non-parametric Mann–Whitney test), N = 10 (Ubxn3b+/+) or N = 6 (Ubxn3b−/−). e The viral titers (mean ± s.e.m) in the brain on day 3 after infection (PFU per gram tissue). **P < 0.01 (non-parametric Mann–Whitney test), N = 5 mice per genotype. The data are pooled from two independent experiments