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

. 2012 Feb 15;23(4):567–576. doi: 10.1091/mbc.E11-09-0781

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

© 2012 Orth et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

“ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology.

PMC Copyright notice

FIGURE 6: — p53 induction after mitotic DNA damage is caspase- and ICAD/CAD-dependent. (A) Immunoblotting of mock, untreated (M) and G2-synchronized (synch) cells, and cells released into K5I showed strong, persistent induction of p53 after release that was significantly blocked by caspase-9 or -7 inhibition. Actin and dynein are loading controls. (B) Live MCF7 p53-Venus cells. First vertical green line in traces is entry into mitotic arrest, second is mitotic slippage. In K5I, p53 is often induced to sustained, high levels. Cells cotreated K5I and zVAD-fmk showed only transient induction of p53 to low levels. RFU, relative fluorescence units. Caspase inhibition resulted in decreased fold induction (average of all cells ± SE) in individual cells and in fewer cells with >2 fold induction. Fold induction is the ratio of the peak intensity to the lowest intensity in each cell. K5I, n = 32; K5I + zVAD-fmk, n = 49. (C) Mock, untreated (M), MCF7, and noncleavable ICAD clone B were G2-synchronized (synch) and released into K5I. When ICAD cleavage is blocked, both p53 induction and DNA damage (γH2A.X) are decreased. Importantly, caspase-7 remains activated after K5I treatment. Dynein is loading control. All blots in each panel are from the same gels and/or samples. (D) Summary of pathway causing DNA damage during mitotic arrest that results in postslippage p53 induction.