REV1 (F6R6I) Rabbit Monoclonal Antibody #56616

Translesion synthesis (TLS) is a DNA damage tolerance mechanism that allows error-prone DNA polymerases to bypass lesions that would otherwise block DNA replication. This bypass prevents replication fork collapse, avoiding genome instability and potentially tumorigenesis. TLS requires specialized DNA polymerases, which in humans include the Y-family polymerases POLη, POLι, POLκ, and REV1, as well as the B-family polymerase POLζ/REV3L (1,2). Targeting TLS is a promising therapeutic strategy in multiple cancers (3).

REV1 is critical for the recruitment and assembly of TLS polymerases at DNA damage sites. The C-terminal domain (CTD) of REV1 is essential for its function, making it a potential therapeutic target (4). Expression of the  REV1 CTD has a dominant negative effect on TLS, sensitizing cancer cells to DNA-damaging agents (5). Additional REV1 inhibitors have been shown to sensitize cancer cells to radiation and chemotherapy (6-8).