Evidence in this study suggested that BBR mediates LPS induced inflammation in HDPF via miR-21/KBTBD7 axis to regulate NF-κB signal pathway, which may provide theoretical basis for BBR in prevention of pulpitis.
Therefore, our findings demonstrate that miR-21 attenuates inflammation, cardiac dysfunction, and maladaptive remodeling post MI through targeting KBTBD7 and inhibiting p38 and NF-κB signaling activation, suggesting that miR-21 may function as a novel potential therapeutic target for MI.
Here, we show that a Cullin 3 (Cul3)/kelch repeat and BTB domain-containing 7 complex controls both the regulated proteasomal degradation of neurofibromin and the pathogenic destabilization of neurofibromin in glioblastomas.