DNA polymerase nu (POLN)

DNA polymerase nu (POLN) is a member of the A-family DNA polymerases that exhibits activity in DNA-templated synthesis, especially in the context of DNA repair and replication bypass of certain lesions[2]. POLN is uniquely capable of translesion synthesis past specific bulky DNA adducts, such as thymine glycol and major groove DNA-protein or DNA-DNA cross-links, but it is blocked by other lesions (e.g., minor groove adducts and some bulky carcinogen adducts)[1]. Unlike replicative DNA polymerases, POLN lacks 3′→5′ exonuclease (proofreading) activity, making its DNA synthesis highly error-prone[1][2]. Functionally, POLN participates in the repair of DNA interstrand cross-links, collaborating with homologous recombination factors and other components of the Fanconi anemia pathway[2]. It interacts with proteins such as RAD51 and HEL308 helicase[2]. POLN is highly regulated in a cell cycle–dependent manner, with protein levels highest during S phase[2]. There are no currently approved or established drugs directly targeting DNA polymerase nu, and its high mutagenicity represents a notable obstacle for direct therapeutic interventions[2].

Other names

POLNDNA polymerase Npol nuPOL4Ppolymerase (DNA directed) nupolymerase (DNA) nu

Not applicable (no characterized drugs targeting this enzyme directly)