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DNA-protein crosslinking can be caused by a variety of chemical and physical agents, including transition metals, ionizing radiation, and endogenous aldehydes, in addition to chemotherapeutic agents. [26] Similar to DNA crosslinking, DNA-protein crosslinks are lesions in cells that are frequently damaged by UV radiation.
Interstrand crosslinks block the progression of DNA replication, and structures at blocked DNA replication forks provide substrates for cleavage by ERCC1-XPF. [23] [24] Incisions may be made on either side of the crosslink on one DNA strand to unhook the crosslink and initiate repair. Alternatively, a double-strand break may be made in the DNA ...
Recombinational repair of DNA double-strand damage - some key steps. ATM (ATM) is a protein kinase that is recruited and activated by DNA double-strand breaks. DNA double-strand damages also activate the Fanconi anemia core complex (FANCA/B/C/E/F/G/L/M). [7] The FA core complex monoubiquitinates the downstream targets FANCD2 and FANCI. [8]
That marked the start of the Schärer lab - researching chemical, biochemical and cell biological approaches to research nucleotide excision repair, interstrand crosslink repair and how DNA repair pathways impact cancer chemotherapy. [7] The last four years of his time in Zürich, he taught biological chemistry as a lecturer at ETH Zürich.
A deficiency of FAN1 increases in vitro sensitivity to cisplatin and mitomycin C, two crosslinking agents [6] [7] FAN1 is also able to repair mitomycin C induced double strand breaks. [7] Germline mutations in the FAN1 gene can cause hereditary colorectal cancer due to defective DNA repair. [20]
Some alkylating agents are active under conditions present in cells; and the same mechanism that makes them toxic allows them to be used as anti-cancer drugs. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate.
DNA crosslinks are caused by numerous anti-cancer drugs (such as cisplatin), but they also must arise naturally since individuals carrying a genetic defect in crosslink repair suffer from the illness Fanconi anaemia. This devastating inherited illness leads to congenital defects, progressive loss of blood production and an enormous lifetime ...
Agata Smogorzewska is a Polish-born scientist. She is an associate professor at Rockefeller University, heading the Laboratory of Genome Maintenance. [1] [2] Her work primarily focuses on DNA interstrand crosslink repair and the diseases resulting from deficiencies in this repair pathway, including Fanconi anemia and karyomegalic interstitial nephritis.
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