{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nREV1 is an indispensable Y‐family translesion synthesis (TLS) DNA polymerase that functions primarily as a scaffold to orchestrate the assembly of specialized TLS enzymes at sites of DNA damage. It interacts with other TLS polymerases—including pol η, pol κ, and pol ι—and with the noncatalytic subunit REV7 to promote a regulated polymerase switch that enables replication to bypass various lesions such as UV‐induced photoproducts and bulky DNA adducts. Structural studies have revealed that its C‐terminal domain provides a versatile platform for binding conserved REV1‐interacting regions (RIRs), which is critical for its role in recruiting and stabilizing repair complexes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its scaffolding role, REV1 exhibits a modest catalytic activity that is largely specific for inserting deoxycytidine monophosphate (dCMP) opposite template lesions such as abasic sites and N²‐modified deoxyguanosine adducts. Detailed biochemical and structural analyses have shown that unique features—including its N‐terminal “N‐digit” and ubiquitin‐binding motifs—contribute to substrate discrimination and binding affinity. These intrinsic properties help promote lesion bypass while coordinating interactions with monoubiquitinated factors at stalled replication forks, thereby ensuring that DNA synthesis can resume despite the presence of damage."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in lesion bypass per se, REV1 serves as a central coordinator of DNA damage tolerance pathways by interfacing with key regulatory factors—including PCNA, RAD18, and other replicative and TLS polymerases—to fine‐tune the balance between error-prone and error-free processes. It participates in multiple aspects of genome maintenance: from modulating the replication of challenging structures like G-quadruplex DNA and facilitating double-strand break repair to influencing cellular responses to chemotherapeutic agents. Changes in REV1 expression levels or mutations within its interaction domains have been linked to altered mutagenesis rates, chemoresistance (e.g. to cisplatin), and cancer susceptibility, underscoring its potential as a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Eiji Ohashi, Yoshiki Murakumo, Naoko Kanjo, et al. 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