Date published: 2025-9-15

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Atm Activators

Atm Activators are a unique class of chemicals focused on modulating the activity of ATM serine/threonine kinase, a critical protein in the DNA damage response pathway. These activators are diverse in their mechanisms but ultimately lead to the activation of Atm, generally through the induction of DNA damage or alteration in cellular redox status. For example, Hydroxyurea and Etoposide induce DNA double-strand breaks, a form of DNA damage that is directly recognized by Atm, thereby activating it. Similarly, Doxorubicin and Bleomycin also function by causing DNA damage, which in turn calls Atm into action. In contrast, agents like N-Acetylcysteine (NAC) and Arsenic Trioxide affect Atm indirectly. NAC is known to promote detoxification of reactive oxygen species, thereby indirectly promoting Atm activation through redox regulation. Arsenic Trioxide also induces oxidative stress, which is a potent trigger for Atm activation.

Curcumin and Sodium Arsenite further broaden the spectrum of mechanisms. Curcumin activates Atm by inducing both DNA damage and oxidative stress. Sodium Arsenite, much like Arsenic Trioxide, causes DNA damage, but through a different mechanism involving double-strand break recognition. It's worth noting that not all chemicals typically considered Atm activators do so by direct activation. Caffeine, for instance, modulates Atm by inhibiting its auto-phosphorylation but sensitizes the protein for activation by other means. The cumulative effect of these chemicals is the activation or sensitization of Atm to carry out its function in DNA damage recognition and repair, along with other cellular processes that require its involvement. These chemicals, therefore, provide multiple routes for influencing Atm activation, each with its unique mechanism and impact.

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