Does nF-κB induce miR-148a to sustain TGF-β/Smad signaling activation in glioblastoma?
These findings uncover a plausible mechanism for NF-κB-sustained TGF-β/Smad activation via miR-148a in glioblastoma, and may suggest a new target for clinical intervention in human cancer.
GABRA1 functional mutations or polymorphisms are not associated with the intrinsic mechanism of GDPP in girls with and without EEG abnormalities.