ArticlemicroPublication biology2022
KAT5 histone acetyltransferase mutations in cancer cells.
Article in microPublication biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 4 citations in OpenAlex.
- Microenvironment-derived acetylated amino acids promote glioblastoma treatment resistance.Research square · 2026Article
- CRISPR/Cas9 Screening Highlights PFKFB3 Gene as a Major Contributor to 5-Fluorouracil Resistance in Esophageal Cancer.Cancers · 2025Article
- In silico protein structural analysis of PRMT5 and RUVBL1 mutations arising in human cancers.Cancer genetics · 2025Article
- Article
- Chromodomain mutation in S. pombe Kat5/Mst1 affects centromere dynamics and DNA repair.PloS one · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells are characterized by accumulation of mutations due to improperly repaired DNA damage. The DNA double strand break is one of the most severe form of damage and several redundant mechanisms have evolved to facilitate accurate repair. During DNA replication and in mitosis, breaks are primarily repaired by homologous recombination which is facilitated by several genes. Key to this process is the breast cancer susceptibility genes BRCA1 and BRCA2 as well as the accessory RAD52 gene. Proper chromatin remodeling is also essential for repair and the KAT5 histone acetyltransferase facilitates histone removal at the break. Here we undertook a pan cancer analysis to investigate mutations within the KAT5 gene in cancer cells. We employed two standard artificial algorithms to classify mutations as either driver (CHASMPlus algorithm) or pathogenic (VEST4 algorithm). We find that most predicted driver and disease-causing mutations occur in the catalytic site or within key regulatory domains.
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.