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

. 2014 Aug 1;7:53. doi: 10.1186/s13045-014-0053-9

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

Copyright © 2014 Qi et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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.

PMC Copyright notice

Proposed mechanisms for the anti-leukemic interaction of MK-1775 and LY2603618 in AML cells. MK-1775 inhibits Wee1, leading to decreased inhibitory phosphorylation of CDK1/2, allowing CDK1/CDK2 to remain active. This eventually leads to DNA DSBs which triggers activation of ATM/ATR and activates CHK1. Active CHK1 inhibits CDC25s leading to decreased removal of the inhibitory phosphorylation on CDK1/2, thus limiting the amount of active CDK1/2 and the resulting DNA damage from MK-1775 treatment. The addition of a CHK1 inhibitor (e.g. LY2603618) would inhibit the CHK1 DNA repair pathway, allowing for the DNA damage to accumulate and cause apoptosis.