We found that the V protein significantly promotes viral replication. To further elucidate the mechanism of the V protein regulating BPIV3 function, a BPIV3 mutant with the V protein deleted (BPIV3-VS
HEK293T ishXrn1 cells were treated with doxycycline for 3-4 days to induce knock down of Xrn1, then transfected with the luciferase reporters containing 99 bp insertions from the STOML2 or YKT6, and T
Immunofluorescence of NF-κB subunit p65 (green fluorescence – FITC) and actin filaments (F-actin, red fluorescence – ActinRed555) expressed in human dental pulp cells (HDPCs) after one and seven days
14-3-3 sigma with RelA/p65 binding site pS45 and covalently bound TCF521-153 Descriptor: 14-3-3 protein sigma, 4-nitro-3-[(3S)-3-oxidanylpiperidin-1-yl]benzaldehyde, Transcription factor p65 Authors:
