Cell Cycle Regulation
There are three major regulatory cell cycle checkpoints - at the G1/S boundary, in the S-phase and during G2/M phases. A cell can only pass through these checkpoints in the presence of stimulatory signals and in the absence of DNA damage. If DNA damage cannot be repaired the cell is eliminated through apoptosis. Cyclin-dependent kinases (Cdks), along with cyclins, are major control switches at these checkpoints. They are central to cell cycle control; their activation via cyclin mediates progression through all four phases of the cell cycle.
p53 is a protein that functions to block the cell cycle if the DNA is damaged. If the damage is severe this protein can cause apoptosis. p53 levels are increased in damaged cells, blocking the cell cycle and allowing time for DNA repair to occur.
Cell Cycle and Cancer
Mutations in proteins controlling the cell cycle can lead to uncontrolled cell division, resulting in cancer - a disease where regulation of the cell cycle goes awry and normal cell growth and behavior is lost. A p53 mutation is the most frequent mutation leading to cancer. Understanding the processes and signaling pathways involved in the cell cycle has thus become the focus of intense interest in cancer research.View all products for Cell Cycle »
Literature for Cell Cycle
A collection of over 750 products for cancer research, the guide includes research tools for the study of:
- Cancer Metabolism
- Epigenetics in Cancer
- Receptor Signaling
- Cell Cycle and DNA Damage Repair
- Invasion and Metastasis
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.Request copy | Download PDF | View all posters
Written by Christopher J. Brown et al, this poster highlights the main strategies that may be utilized to reactivate p53, that is found to be frequently mutated and inactivated in tumors. It focuses on small molecules and peptides which act to stabilize p53 and rescue wild-type activity. Compounds available from Tocris are listed.Request copy | View all posters
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