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. 2019 Oct 16;21:213. doi: 10.1186/s13075-019-1990-z

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Notch inhibited TNF-α-promoted apoptosis via Fas. a, b Fas and RIP mRNA expression levels were upregulated by TNF-α stimulation and downregulated by JAG2 treatment; TUNEL assay showed similar results. c–g Western blot analysis showed that Fas, RIP1, cleaved-caspase-8, and cleaved-caspase-3 protein expression levels were upregulated by TNF-α and downregulated by JAG2 treatment; Notch2/Hes1/Hey2 siRNA significantly enhanced the induction by TNF-α. h, i The apoptotic mortality of cultured NP cells caused by TNF-α with or without Notch2/Hey2/Hes1 siRNA treatment was reduced by the addition of anti-FasL antibody to the culture. P values were computed vs. non-stimulated controls*, TNF-α-stimulated controls^#, or JAG2-stimulated controls^&; *^,#,&P < 0.05