Loading
Life sciences · Journal article
Biomolecules · October 20, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Genomic DNA is constantly exposed to endogenous and exogenous stresses that can cause different types of DNA damage. DNA double-strand breaks (DSBs) are among the most damaging forms of DNA lesions, as persistent breaks can compromise genome stability. In response to such damage, cells activate DNA damage response (DDR) pathways that detect lesions and promote their repair. Lysine lactylation (Kla), a recently identified lysine acylation modification, links cellular metabolism and DNA repair. Recent evidence suggests that Kla may influence DDR by modulating the stability, interactions, and activity of DNA repair proteins. This review discusses recent advances in our understanding of lactylation in homologous recombination (HDR) and non-homologous end joining (NHEJ). We focus on MRE11, NBS1, BLM, and XLF lactylation and their roles in DNA repair and tumor chemoresistance. These findings suggest that lactylation can affect genome stability, tumor progression, and responses to cancer therapy by regulating key DDR factors. However, how lactylation is regulated during DDR and how it affects DNA repair remain largely unclear. Further studies are needed to elucidate how DNA damage-induced lactylation can be regulated, the functions of lactylation writers and erasers, and the significance of lactylation in various disease contexts.