ArticleNucleic acids research2026
KIF2A-mediated microtubule-dependent nuclear envelope invagination drives nonhomologous end joining.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
The spatial distribution and dynamics of double-strand break (DSBs) repair controlled by microtubules are essential for preserving genomic stability. However, the processes through which extranuclear microtubules govern intranuclear DSB repair across the nuclear envelope (NE) remain poorly understood. This study uncovers a mechanism by which the microtubule-depolymerizing kinesin KIF2A regulates nonhomologous end joining (NHEJ) repair by mediating NE invagination. Our investigation reveals that damage-induced α-tubulin tyrosination triggers KIF2A binding to microtubules, subsequently inducing NE invagination through the microtubule-the linker of nucleoskeleton and cytoskeleton (LINC) complex and lamin B1. This invagination, in turn, provides a larger region of a stable NHEJ repair environment close to the NE, facilitating efficient NHEJ repair. Loss of KIF2A disrupts the formation of invaginations after DNA damage, impacting the formation of 53BP1 foci. Our study establishes KIF2A-mediated NE invagination as a critical regulator of the intricate relationships among microtubules, NE dynamics, and NHEJ repair, shedding light on a previously obscure pathway crucial for genome stability.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.