{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nREV3L encodes the catalytic subunit of DNA polymerase ζ—a specialized B‐family DNA polymerase that mediates translesion synthesis (TLS) by allowing DNA replication to continue past diverse DNA lesions such as ultraviolet photoproducts, cisplatin‐induced cross‐links, and bulky adducts. In this process, REV3L partners with accessory proteins such as REV7 (and in some cases with PolD2 and PolD3) to execute the extension step following lesion bypass. This complex error‐prone mechanism is essential for tolerating DNA damage that would otherwise stall high‐fidelity replicative polymerases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical TLS activity, REV3L plays a critical role in maintaining genomic stability. Its function ensures proper replication fork progression through problematic DNA regions—including common fragile sites—and facilitates the repair of double‐strand breaks and complex DNA lesions. Disruption of REV3L (or its regulatory interactions) leads to replication stress, chromosomal aberrations, cell cycle arrest, and embryonic lethality in mammals. These findings highlight a developmentally essential role for REV3L and its contribution to the fidelity of DNA replication and repair."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, aberrant regulation of REV3L is increasingly linked to cancer development and chemoresistance. Elevated REV3L expression—observed in several tumor types such as glioma, cervical cancer, and non‐small cell lung cancer—can promote resistance to DNA cross‐linking agents and cisplatin by facilitating error‐prone TLS; conversely, REV3L downregulation sensitizes cancer cells to these agents and leads to cellular growth arrest or apoptosis. REV3L levels and activity are further modulated by post‐translational processes (including proteolytic cleavage that protects it from degradation), microRNA‐mediated regulatory mechanisms, and even mitochondrial localization that influences metabolic and invasive properties. Structural studies have begun to elucidate how REV3L interacts with key partners (e.g. REV7 and REV1) to coordinate polymerase switching at stalled replication forks. Collectively, these findings position REV3L as a pivotal factor in the cellular response to DNA damage and present its modulation as a promising avenue for improving therapeutic outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ziqiang Li, Hong Zhang, Terrence P McManus, et al. "}, {"type": "b", "children": [{"type": "t", "text": "hREV3 is essential for error-prone translesion synthesis past UV or benzo[a]pyrene diol epoxide-induced DNA lesions in human fibroblasts."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mutat Res (2002)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/s0027-5107(02)00253-1"}], "href": "https://doi.org/10.1016/s0027-5107(02"}, {"type": "t", "text": "00253-1) PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12459444"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12459444"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Feng Zhu, Cai-Xia Jin, Tao Song, et al. 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