Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Nov 2;119(12):1538–1551. doi: 10.1038/s41416-018-0265-9

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 4 — NGLY1 suppression enhanced the production of IFNβ1 and IL-29 that contributes to viability reduction in melanoma cells. (a) The contents of IFNβ1 and IL-29 in the conditioned media of UACC257 and SK-MEL-2 cell clones with the indicated treatment were measured by cytokine profiling. (b) The NGLY1 knockdown-induced upregulation of IFNβ1 and IL-29 was significantly attenuated by the overexpression of exogenous human NGLY1 in the cells. (c) Left panel: the attenuation of NGLY1 knockdown-induced viability reduction by the treatment of specific IFNβ1 neutralisation antibody in the cells. Right panel: the attenuation of NGLY1 knockdown-induced viability reduction by the treatment of specific IL-29 neutralisation antibody in the cells. NGLY knockdown was induced by the treatment of 2 µM dox for 72 h in the cells. (d) The enhanced expression and activation of IRF3, IRF7 and their upstream kinase TBK1 was detected in SK-MEL-2 and MALME3M cells with NGLY1 knockdown. The serine phosphorylation of IRF3 and TBK1 indicates their activity. NT: non-targeting shRNA. 645: NGLY1-targeting shRNA645. All data were presented as mean ± standard deviation (n = 3; *P < 0.05, t-test)