We believe the large and highly significant effects we see on Ripk3 transcription and on RIPK3-mediated cell death in HUVECs following NF�B1 knockdown and TNF� stimulation are more compelling than the nominal changes we saw in baseline MS1 cells with NF�B1 manipulation.
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Genomic locus proteomic screening identifies the NF-κB signaling pathway components NFκB1 and IKBKG as transcriptional regulators of Ripk3 in endothelial cells.
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