PMC:7025468 / 37874-38671 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7025468","sourcedb":"PMC","sourceid":"7025468","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7025468","text":"Here, we demonstrate that Meth can induce expression of IL-1β and miR-146a in CD4+ T-cells, with overexpression of the cytokine leading to increased expression of miR-146a. Meth mediated miR-146a overexpression targeted TRAF6 to modulate innate immune signaling pathways. Based on our findings, we hypothesized that IL-1β signaling results in increased IL-1β mRNA levels and increased miR-146a expression. We further hypothesized that IL-1β-dependent induction of miR-146a would target key innate immune pathways by decreasing TRAF6 expression (Figure S2). Although there are several known targets of miR-146a, only TRAF6 was significantly affected during Meth treatment. We also observed that induction of an IL-1β auto-regulatory loop contributed to Meth mediated increases in HIV-1 replication.","tracks":[]}