Dclre1c Activators

DCLRE1C, a key player in V(D)J recombination and DNA repair, exhibits single-strand-specific 5'-3' exonuclease and endonuclease activities on various DNA structures. Mutations in this gene can lead to severe combined immunodeficiency (SCID) and Omenn syndrome. Activation of DCLRE1C is crucial for its role in maintaining genomic integrity and responding to DNA damage. DCLRE1C is directly activated by genotoxic chemicals like camptothecin, etoposide, and bleomycin, inducing DNA damage and promoting its engagement in DNA repair and V(D)J recombination. Mitomycin C and cisplatin activate DCLRE1C by inducing DNA cross-links, highlighting its role in recognizing and processing diverse DNA lesions. Additionally, chemicals such as hydroxyurea and aphidicolin activate DCLRE1C by inducing replication stress, emphasizing its contribution to maintaining genomic stability during DNA replication challenges.

The general mechanisms of activation involve the recognition and processing of specific DNA structures generated by genotoxic stress. DCLRE1C acts as a guardian of genomic integrity, responding to challenges in DNA structure and replication. The diverse array of activators reflects the intricate regulatory network that ensures a robust and specific cellular response to different types of DNA damage. Understanding the activation mechanisms of DCLRE1C contributes to the knowledge of DNA repair processes and potential interventions for associated genetic disorders.