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Cells have evolved two main repair pathways to suppress the formation of these genotoxic lesions: homology-dependent, error-free homologous recombination repair (HRR), and potentially error-prone, classical, DNA-PK-dependent non-homologous end-joining (c-NHEJ).
The repair of MMC-induced DNA lesions involves multiple DNA repair pathways, with HR and other HR-dependent DNA repair pathways, i.e. Fanconi anaemia (FA) and nucleotide-excision repair (NER), being the main repair pathways [19].
Recognition and repair of DSBs is a complex and dynamic process involving at least two main repair pathways, non-homologous end joining (NHEJ) and homologous recombination (HR) repair.
Error prone, nonhomologous end joining (NHEJ) and high fidelity, error‐free homologous recombination (HR) are the two main repair pathways for DSB.
Although the main repair pathways have been identified and characterized using genetic, biochemical, biophysical, and cell biological approaches, we are still far from understanding the overall organization of DNA repair in cells.
Given the role of DNA repair in the radioresponse of human tumour cells and the presence of two main repair pathways, we previously studied the role of DNA-PK-dependent NHEJ in the radiosensitivity of non-small-cell lung cancer (NSCLC) and have shown that reduced DNA-PK activity decreased the rejoining of radiation-induced DNA Dsb and increased the radiosensitivity (Sak et al, 2002).
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Interestingly, Pif1 has been shown to have a critical role repair of DSBs where break-induced replication (BIR) is the main repair pathway (Chung et al, 2010).
In this bacterium, RecD is the only member that is identified in the RecBCD pathway, whereas all of the members associated with the RecFOR pathway have been found in the genome of D. radiodurans, suggesting that the RecFOR pathway is the main repair pathway of DNA damage in this organism [ 9].
In mammals, at least two main DSB repair pathways have evolved, namely non-homologous end joining (NHEJ) and homologous recombination (HR).
There are two main DSB repair pathways, the Homologous Recombination (HR) and the Non-Homologous End Joining (NHEJ) which are conserved in eukaryotes from yeast to human [1], [2].
Specific genes representative of the main DNA repair pathways in human beings were examined.
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