cell cycle arrest
Definition
Cell cycle arrest is a regulatory mechanism that halts progression through the cell cycle at specific checkpoints (G1/S, G2/M, or spindle checkpoints) in response to cellular stress, DNA damage, or developmental signals. This process prevents cells from replicating damaged genetic material or dividing under unfavorable conditions. Key mediators include checkpoint kinases (CHK1, CHK2), cyclin-dependent kinase inhibitors (p21, p27), and tumor suppressors like p53. Cell cycle arrest can be temporary, allowing time for DNA repair, or permanent (senescence). Understanding arrest mechanisms is crucial for cancer research, as malignant cells often bypass these checkpoints, and many chemotherapeutic agents function by inducing arrest.
Visualize cell cycle arrest in Nodes Bio
Researchers can map cell cycle arrest pathways by visualizing interactions between checkpoint proteins, CDKs, cyclins, and upstream stress signals. Network analysis reveals how DNA damage sensors connect to arrest effectors, identifies feedback loops maintaining arrest states, and shows crosstalk between different checkpoint pathways. Causal inference tools help distinguish direct regulators from downstream consequences in arrest signaling cascades.
Visualization Ideas:
- Checkpoint signaling cascades showing DNA damage sensors to CDK inhibition
- Multi-checkpoint network comparing G1/S versus G2/M arrest pathways
- Drug-induced arrest mechanisms with compound-target-phenotype relationships
Example Use Case
A pharmaceutical team investigating a novel kinase inhibitor observes G2/M arrest in cancer cells. Using network visualization, they map the compound's effects on ATR-CHK1-WEE1 signaling and downstream CDK1 inhibition. The analysis reveals unexpected activation of p38 MAPK stress pathways and identifies compensatory survival signals through AKT phosphorylation. This network view guides combination therapy strategies, suggesting co-treatment with AKT inhibitors to prevent escape from arrest and enhance therapeutic efficacy.