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| NHEJ - Non-Homologous End Joining Abbreviation: NHEJ, c-NHEJ Type: DNA double-strand break repair pathway / DNA damage response process Function: NHEJ repairs DNA double-strand breaks by directly recognizing, processing, and ligating broken DNA ends without requiring a homologous DNA template. It is a major double-strand break repair pathway in mammalian cells and is particularly active during G0/G1. Because DNA ends may require processing before ligation, NHEJ can introduce small insertions or deletions at the repaired junction. Major Components: KU70/XRCC6, KU80/XRCC5, DNA-PKcs/PRKDC, Artemis/DCLRE1C, XRCC4, XLF/NHEJ1, PAXX, and DNA Ligase IV/LIG4. Cancer: ↕ Context-dependent. Normal NHEJ protects genomic integrity by repairing potentially lethal DNA double-strand breaks. However, established cancer cells can exploit NHEJ to survive radiation, replication-associated damage, and DNA-damaging chemotherapy, contributing to treatment resistance. Favorable Direction in Cancer: Context-dependent. ↓ NHEJ activity can be favorable during radiation or DNA-damaging therapy by preventing repair of treatment-induced double-strand breaks, whereas severe loss of NHEJ in normal cells can increase genomic instability and cancer risk. Interpretation Note: Classical NHEJ should be distinguished from alternative end joining (alt-EJ/MMEJ/TMEJ), which uses different proteins and often relies on short regions of microhomology. |
| 8265- | LE, | Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response |
| - | vitro+vivo, | CRC, | NA |
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