Date published: 2025-10-11

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FANCA Activators

The term FANCA Activators refers to a group of chemicals and agents that, while not directly designed to target or activate the FANCA protein, play crucial roles in triggering the cellular response pathways in which FANCA participates. FANCA, a component of the Fanconi anemia pathway, is instrumental in maintaining genomic stability and repairing DNA damage. Therefore, the activation of FANCA is essential for preserving the integrity of the genetic material within cells.

Mitomycin C, for instance, is an agent that forms DNA cross-links, primarily interstrand cross-links. When these cross-links occur, cells recognize them as DNA lesions and initiate a sophisticated cellular response. FANCA is one of the key players in this response, as it helps orchestrate the repair of these cross-links. Similarly, cisplatin, another chemotherapy drug, creates covalent DNA adducts and cross-links, thus indirectly activating FANCA as part of the cellular effort to rectify the DNA damage. These chemicals, by inducing DNA damage that necessitates repair, indirectly stimulate FANCA and other Fanconi anemia pathway components. Hydrogen peroxide (H2O2) and ionizing radiation are agents that induce oxidative stress and DNA damage, including double-strand breaks. In response to such damage, cells activate FANCA and the Fanconi anemia pathway to repair these lesions. Phorbol 12-myristate 13-acetate (PMA) and menadione can activate the Fanconi anemia pathway, including FANCA, by promoting DNA repair processes in response to various types of DNA damage, whether oxidative or otherwise. Camptothecin and 5-fluorouracil (5-FU) interfere with DNA replication and cause DNA damage, indirectly activating FANCA as part of the cellular response to replication stress. Etoposide, hydroxyurea, bleomycin, and methyl methanesulfonate (MMS) induce DNA damage of various types, and FANCA is indirectly activated as cells initiate DNA repair mechanisms in response to these injuries.

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