First-pass extracted concept

non-homologous end joining

Candidate: concept label3 source documents8 linked claims
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Aliases

NHEJ

Extracted Explainers

What the tool is doing

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.

Source 3DOIPubMed

What problem it solves

It addresses repair of ionizing-radiation-induced DNA double-strand breaks and supports V(D)J recombination during adaptive immune development.

Source 3DOIPubMed

What it does not solve

The abstract does not compare NHEJ performance against all other repair pathways or define when it fails.

Source 3DOIPubMed

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.
Evidence 1Source 1DOIPubMedprovenance
non-homologous end joining (NHEJ), which often results in mutations such as deletions or frameshift errors
Evidence 2Source 2DOIPubMedprovenance
Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation-induced DNA double-strand breaks (DSBs) in human cells...
Evidence 3Source 3DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1disease relevancesupports2026Source 1DOIPubMed

Dysregulation in the NHEJ pathway contributes to genomic instability, oncogenesis, and resistance to genotoxic therapies.

Quoted textsource-backed
Dysregulation in the NHEJ pathway contributes to genomic instability, oncogenesis, and resistance to genotoxic therapies.
Claim 2mechanismsupports2026Source 1DOIPubMed

NHEJ is a critical DSB repair pathway that operates throughout the cell cycle and does not require a homologous template.

Quoted textsource-backed
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
Claim 3therapeutic strategysupports2026Source 1DOIPubMed

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.

Quoted textsource-backed
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.
Claim 4mechanism rolesupports2025Source 2DOIPubMed

Gene editing techniques depend on HDR and NHEJ as two main DNA repair mechanisms.

Quoted textsource-backed
These techniques depend on two main DNA repair mechanisms: homology-directed repair (HDR) ... and non-homologous end joining (NHEJ)
Claim 5mechanistic propertysupports2025Source 2DOIPubMed

NHEJ often results in mutations such as deletions or frameshift errors.

Quoted textsource-backed
non-homologous end joining (NHEJ), which often results in mutations such as deletions or frameshift errors
Claim 6biological requirementsupports2023Source 3DOIPubMed

Non-homologous end joining is essential for generation of mature T and B cells via V(D)J recombination.

Quoted textsource-backed
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
Claim 7mechanistic modelsupports2023Source 3DOIPubMed

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.

Quoted textsource-backed
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.
Claim 8pathway rolesupports2023Source 3DOIPubMed

Non-homologous end joining is the major pathway for repair of ionizing-radiation-induced DNA double-strand breaks in human cells.

Quoted textsource-backed
Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation-induced DNA double-strand breaks (DSBs) in human cells