DNA-dependent protein kinase (DNA-PK) is a nuclear protein serine/threonine kinase that is a molecular sensor of DNA damage. DNA-PK is involved in the ligation step of the non-homologous end joining (NHEJ) pathway of DNA double strand break (DSB) repair.
Inhibitors |
Cat. No. | Product Name / Activity |
---|---|
3271 | Compound 401 |
Selective DNA-PK and mTOR inhibitor | |
4702 | ETP 45658 |
DNA-PK inhibitor; also inhibits PI 3-K and mTOR | |
4840 | KU 0060648 |
Dual DNA-PK and PI 3-K inhibitor | |
5834 | LTURM 34 |
Potent DNA-PK inhibitor | |
2828 | NU 7026 |
Selective DNA-PK inhibitor | |
3712 | NU 7441 |
Potent and selective DNA-PK inhibitor | |
6792 | Omipalisib |
Potent DNA-PK inhibitor; also inhibitor of mTOR and highly potent inhibitor of PI 3-kinase | |
2930 | PI 103 hydrochloride |
Inhibitor of DNA-PK, mTOR and PI 3-kinase |
DNA-dependent protein kinase (DNA-PK) is a nuclear protein serine/threonine kinase that is a molecular sensor of DNA damage. DNA-PK is involved in the ligation step of the non-homologous end joining (NHEJ) pathway of DNA double strand break (DSB) repair, V(D)J recombination and telomere stabilization.
DNA-PK is activated by phosphorylation by ATM/ATR following DNA damage and is inhibited by wortmannin. DNA-PK must be bound to DNA in order to exhibit its catalytic properties and has multiple targets including c-Abl, histone H1, c-jun, p53, c-Myc and more.
Tocris offers the following scientific literature for DNA-Dependent Protein Kinase to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.