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Fig. 4 | Retrovirology

Fig. 4

From: p30 protein: a critical regulator of HTLV-1 viral latency and host immunity

Fig. 4

p30 inhibits homologous recombination repair in favor of nonhomologous end-joining repair. DNA damage is an event that is commonly caused by interaction with chemical radicals, produced as a result of cellular metabolism, or by external damaging agents such as ionizing radiations. The broken DNA molecule (black) invades an undamaged homologous molecule (blue) that is used as a template to repair the damage. Repair synthesis is characterized by branch migration, and resolution involving cutting of the junctions between the two molecules (black and blue). The p30 viral protein interacts with the members of the MRN complex, NBS1, and Rad50, essential for the initiation of homologous recombination repair. In the presence of p30, HR repair is impaired, and the DNA double-strand breaks are preferentially repaired through the error-prone NHEJ, which might lead to genetic mutations

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