NHEJ repairs DNA double-strand breaks in human cells. The review frames it as a pathway that assembles repair complexes at broken DNA ends and progresses toward ligation.
First-pass extracted concept
non-homologous end joining
Aliases
NHEJ
Extracted Explainers
What the tool is doing
What problem it solves
Evidence Snippets
Non-homologous end joining (NHEJ) is a critical DNA double-strand break (DSB) repair pathway that operates throughout the cell cycle to maintain the genomic stability of the cell.
non-homologous end joining (NHEJ), which often results in mutations such as deletions or frameshift errors
Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation-induced DNA double-strand breaks (DSBs) in human cells...
Supporting Sources
Linked Claims
Dysregulation in the NHEJ pathway contributes to genomic instability, oncogenesis, and resistance to genotoxic therapies.
Dysregulation in the NHEJ pathway contributes to genomic instability, oncogenesis, and resistance to genotoxic therapies.
NHEJ is a critical DSB repair pathway that operates throughout the cell cycle and does not require a homologous template.
Non-homologous end joining (NHEJ) is a critical DNA double-strand break (DSB) repair pathway that operates throughout the cell cycle to maintain the genomic stability of the cell. Unlike homologous recombination (HR), NHEJ is capable of repairing DSBs without the need for a homologous template
Implementation of DNA-PK inhibitors in medical practice could stratify patients based on tumor vulnerability to NHEJ disruption and support combination with radiation or DNA-damaging chemotherapy.
The implementation of DNA-PK inhibitors into medical practice can enable the stratification of oncologic patients into two categories, based on the tumors' vulnerability to NHEJ disruptions. Thus, the therapeutic pathways of patients with NHEJ tumors could branch, combining traditional genotoxic therapies (radiation and DNA-damaging chemotherapeutics) with DNA-PK inhibitors to achieve an enhanced effect and improved survival outcomes.
Gene editing techniques depend on HDR and NHEJ as two main DNA repair mechanisms.
These techniques depend on two main DNA repair mechanisms: homology-directed repair (HDR) ... and non-homologous end joining (NHEJ)
NHEJ often results in mutations such as deletions or frameshift errors.
non-homologous end joining (NHEJ), which often results in mutations such as deletions or frameshift errors
Non-homologous end joining is essential for generation of mature T and B cells via V(D)J recombination.
and is essential for the generation of mature T and B cells in the adaptive immune system via the process of V(D)J recombination
Recently determined structures explain how NHEJ proteins assemble to detect and protect DNA double-strand break ends and then proceed through DNA-PKcs-dependent autophosphorylation to a ligation-competent complex.
Together, these studies provide an explanation for how NHEJ proteins assemble to detect and protect DSB ends, then proceed, through DNA-PKcs-dependent autophosphorylation, to a ligation-competent complex.
Non-homologous end joining is the major pathway for repair of ionizing-radiation-induced DNA double-strand breaks in human cells.
Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation-induced DNA double-strand breaks (DSBs) in human cells