Alexa Fluor® 594 Anti-LIG1 antibody [EPR12464]

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

The 'LIG1' protein also known as DNA ligase I plays an important role in DNA replication and repair. Mechanically LIG1 is responsible for catalyzing the formation of phosphodiester bonds between adjacent DNA strands an essential step for sealing Okazaki fragments during lagging strand synthesis. This protein features a molecular weight of approximately 102 kDa. LIG1 is predominantly expressed in the nucleus of proliferating cells with presence noted in various tissues including those undergoing rapid cell division.

Biological function summary

DNA ligase I which is sometimes part of larger DNA replication complexes ensures the faithful duplication and repair of the genome. This protein assists with repairing single and double-strand breaks thereby maintaining genomic stability. In the context of DNA replication LIG1 is necessary for completing the joining of discontinuous segments preventing loss of genetic information. Mutations or deficiencies can compromise this repairing process potentially leading to genome instability.

Pathways

LIG1 participates in the DNA replication pathway and the base excision repair pathway. Within these pathways LIG1 interacts with other proteins such as proliferating cell nuclear antigen (PCNA) to facilitate its recruitment to DNA and enhance its ligation efficiency. Additionally LIG1 associates with replication factor C (RFC) which acts as a clamp loader and flap endonuclease 1 (FEN1) during DNA replication and repair ensuring proper genome maintenance.

Defective LIG1 function relates to genomic instability which can contribute to conditions such as immunodeficiency and increased cancer susceptibility. For example mutations in the LIG1 gene have been associated with Ligase I deficiency which presents with hypersensitivity to DNA-damaging agents and immunodeficiency. LIG1's activity is also connected to Bloom syndrome where defective DNA repair leads to chromosomal instability involving interactions with proteins such as the Bloom syndrome protein (BLM).