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 Apr 11;7:835. doi: 10.1038/s41598-017-00947-6

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

PID1 in chemotherapy-induced medulloblastoma and glioma apoptosis. The data suggest that PID1 contributes to chemotherapy-induced apoptosis through an NFκB-dependent mechanism as follows: Etoposide and cisplatin both increase PID1 mRNA via NFκB and both increase apoptosis. While etoposide increases both PID1 mRNA and PID1 protein, cisplatin increased PID1 mRNA, but decreased PID1 protein. The cisplatin-induced decrease in PID1 protein is reversed by bortezomib, suggesting that it is due to proteasomal degradation. It is likely that both etoposide and cisplatin activate additional signaling pathways that contribute to apoptosis.