Vitamin D receptor activation in microglia suppresses NOX2-mediated oxidative damage via PAT1 in vitro and in vivo Further, calcitriol or PAT1 deficiency attenuated LPS-induced PAT1 and p47phox membrane translocation (Figure 3B and Figure S2A-F). In parallel, membrane levels of the NADPH oxidase p47phox subunit were also increased following LPS stimulation, whereas PAT1 gene interference had a similar inhibitory effect on LPS-induced membrane translocation to calcitriol treatment (Figure 2B and Figure S1A-D). Accordingly, calcitriol treatment or PAT1 deficiency significantly decreased NADPH oxidase activity induced by LPS. [Extracted from the article]