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

. 2017 Dec 19;7:17761. doi: 10.1038/s41598-017-18087-2

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

© The Author(s) 2017

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

Proposed model of NS1-induced nucleolar stress. Interaction of H3N2/NS1 with NCL compromises NCL association with rRNA gene and results in hyper-methylation state of UCE region of rRNA gene promoter. Hyper-methylated UCE leads to reduced recruitment of RNA Pol I to rRNA gene promoter and inhibition of rRNA transcription, which represses rRNA synthesis, and thereby induces nucleolar stress. Under this rRNA shortage circumstance, free ribosomal proteins interact with MDM2 E3 ubiquitin ligase. The interaction abolishes the negative regulation capacity of MDM2 towards p53 and leads to p53 accumulation, then triggers cell apoptosis.