ReviewInternational journal of molecular sciences2022
The Role of the TSK/TONSL-H3.1 Pathway in Maintaining Genome Stability in Multicellular Eukaryotes.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed, 11 citations in OpenAlex.
- Identification of novel genes with enriched expression in human intermediate progenitors reveals a key role for CDKN3 in cortical development.Stem cell reports · 2026Article
- Comprehensive Bioinformatic Analysis of TONSL Expression in Pan-Cancer.Cancer reports (Hoboken, N.J.) · 2026Article
- H3.1K27M-induced misregulation of the TONSOKU-H3.1 pathway causes genomic instability.Nature communications · 2025Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- TONSL promotes lung adenocarcinoma progression, immune escape and drug sensitivity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- Mitotic inheritance of genetic and epigenetic information via the histone H3.1 variant.Current opinion in plant biology · 2023Review
- Drug Discovery Targeting Post-Translational Modifications in Response to DNA Damages Induced by Space Radiation.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Replication-dependent histone H3.1 and replication-independent histone H3.3 are nearly identical proteins in most multicellular eukaryotes. The N-terminal tails of these H3 variants, where the majority of histone post-translational modifications are made, typically differ by only one amino acid. Despite extensive sequence similarity with H3.3, the H3.1 variant has been hypothesized to play unique roles in cells, as it is specifically expressed and inserted into chromatin during DNA replication. However, identifying a function that is unique to H3.1 during replication has remained elusive. In this review, we discuss recent findings regarding the involvement of the H3.1 variant in regulating the TSK/TONSL-mediated resolution of stalled or broken replication forks. Uncovering this new function for the H3.1 variant has been made possible by the identification of the first proteins containing domains that can selectively bind or modify the H3.1 variant. The functional characterization of H3-variant-specific readers and writers reveals another layer of chromatin-based information regulating transcription, DNA replication, and DNA repair.
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.