In TNF-stimulated cells, RIPK1 promotes cell survival by stabilizing TRAF2 and cIAP1, which limits induction of non-canonical NF-κB and activation of caspase-8.

Abstract

There were several errors in this article. PAGE 13284:The figure legend of with 100 ng/ml Fc-TNF for 0, 5, and 15 min. Cells were then lysed in DISC lysis buffer and split into soluble and insoluble fractions. 25 g of protein from both fractions were run on SDS-PAGE and analyzed for levels of indicated proteins by Western blotting analysis." An asterisk denotes a nonspecific band. PAGE 13285:In the figure legend for Fig. 2A, the text "Keratinocytes were isolated from day old RIPK Ϫ/Ϫ 1-day-old pups" does not refer to panelA of the figure and should be removed. The corrected text for the description of Fig. 2A should read, "E19 embryos were taken, and thymus was harvested. Thymi were dispersed into single cell suspensions, and half of each was left untreated, whereas the other half was treated with 100 ng/ml Fc-TNF for 1 h. Cells were lysed in DISC lysis buffer and analyzed for TRAF2 and cIAP1 by Western blotting analysis. Genotypes were confirmed by Western blotting analysis and PCR." PAGE 13286:At the end of the figure legend for Fig. 4, the text "To control for NEC-1 activity, L929 cells" does not refer to this figure and should be removed. PAGE 13287:The following sentence should be added to the end of the legend to Fig. 6. "Error bars show S.E. of at least three independent experiments." PAGE 13288:In Fig. 7A, the caspase-8 long exposure immunoblot was incorrectly cropped and the molecular mass of the ␤-actin immunoblot was incorrectly labeled. These errors have been corrected so that there are now six lanes in the caspase-8 (long exposure), and the molecular weight of actin reflects the actual size.The following sentence should be added to the figure legend to supplemental Fig. 2. "Error bars show S.E. of at least three independent experiments."These errors do not affect the results or conclusions of the work.

Sensing of endogenous nucleic acids by ZBP1 induces keratinocyte necroptosis and skin inflammation

“…4D and Fig. S3C), which is in agreement with previous reports (Gentle et al, 2011;Kelliher et al, 1998). Spontaneous ZBP1 activation in RIPK1-deficient keratinocytes did not affect IFNγ-induced gene expression as ISG messenger RNA expression or CXCL10 protein production did not differ between the genotypes ( Fig.…”

The interplay of IKK, NF‐κB and RIPK1 signaling in the regulation of cell death, tissue homeostasis and inflammation

“…73 These results were consistent with the finding that the mRNA expression levels of several NF-κB-dependent pro-survival genes were not reduced in RIPK1-deficient IECs. 73,81,82 These results suggest that RIPK1 counteracts FADD-caspase-8 dependent apoptosis of IECs by inhibiting the degradation of pro-survival proteins including TRAF2 and cIAP1 (Figure 4). 73,81 This finding was consistent with the rapid loss of these pro-survival proteins in RIPK1-deficient MEFs upon TNF stimulation.…”

“…73,81 This finding was consistent with the rapid loss of these pro-survival proteins in RIPK1-deficient MEFs upon TNF stimulation. 73,81,82 These results suggest that RIPK1 counteracts FADD-caspase-8 dependent apoptosis of IECs by inhibiting the degradation of pro-survival proteins including TRAF2 and cIAP1 (Figure 4). The mechanisms by which RIPK1 prevents the degradation of TRAF2, cIAP1 and cFLIP remain elusive, but could be related to a function of RIPK1 in stabilizing complex I.…”

Emerging Roles for Noncanonical NF-κB Signaling in the Modulation of Inflammatory Bowel Disease Pathobiology

“…Mechanistically, a ubiquitin ligase complex consisting of TRAF2, TRAF3, and cIAP1/2 catalyzes the ubiquitination and degradation of NIK (103, 104). This is a potent negative regulatory mechanism, as stabilization of cIAP1 through this multi-protein complex limits downstream non-canonical activity, even during active TNF stimulation (105). cIAP1 and cIAP2 have become increasingly associated with IBD (106).…”