Matches in Nanopublications for { ?s ?p "Because RIP1 and TRAF2 are downstream effectors of the TNF receptor, it is possible that MNNG induces TNF through RIP1 and TRAF2 to trigger cell death. To investigate this possibility, we examined the sensitivity of TNFR1-/- MEF cells to MNNG treatment and found that it is comparable with that of WT MEF cells (Fig. 6c). As expected, TNFR1-/- MEF cells are resistant to TNF-induced cell death (Fig. 6c). These results exclude the possibility that RIP1 and TRAF2 function in the TNF signaling pathway in MNNG-treated cells. " ?g. }
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- _5 value "Because RIP1 and TRAF2 are downstream effectors of the TNF receptor, it is possible that MNNG induces TNF through RIP1 and TRAF2 to trigger cell death. To investigate this possibility, we examined the sensitivity of TNFR1-/- MEF cells to MNNG treatment and found that it is comparable with that of WT MEF cells (Fig. 6c). As expected, TNFR1-/- MEF cells are resistant to TNF-induced cell death (Fig. 6c). These results exclude the possibility that RIP1 and TRAF2 function in the TNF signaling pathway in MNNG-treated cells. " provenance.
- _5 value "Because RIP1 and TRAF2 are downstream effectors of the TNF receptor, it is possible that MNNG induces TNF through RIP1 and TRAF2 to trigger cell death. To investigate this possibility, we examined the sensitivity of TNFR1-/- MEF cells to MNNG treatment and found that it is comparable with that of WT MEF cells (Fig. 6c). As expected, TNFR1-/- MEF cells are resistant to TNF-induced cell death (Fig. 6c). These results exclude the possibility that RIP1 and TRAF2 function in the TNF signaling pathway in MNNG-treated cells. " provenance.