ArticleJournal of the American Chemical Society2016
Global Profiling of Acetyltransferase Feedback Regulation.
Article in Journal of the American Chemical Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 53 citations in OpenAlex.
- Hierarchical small molecule inhibition of MYST acetyltransferases.Nature communications · 2026Article
- ACLY promotes NK cell effector function by regulating glycolysis and histone acetylation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Interactome Profiling of a Lysine Deacetylase Trapping Probe Library Uncovers Crosstalk Between HDAC6 and NF-κB Signaling.Angewandte Chemie (International ed. in English) · 2025Article
- Growth phase diets diminish histone acetyltransferase Gcn5 function and shorten lifespan of Drosophila males.EMBO reports · 2025Article
- NAT10 inhibition promotes ac4C-dependent ferroptosis to counteract sorafenib resistance in nasopharyngeal carcinoma.Cancer science · 2024Article
- FSP1-mediated ferroptosis in cancer: from mechanisms to therapeutic applications.Apoptosis : an international journal on programmed cell death · 2024Review
- Regulation of proteostasis and innate immunity via mitochondria-nuclear communication.The Journal of cell biology · 2024Review
- NAT10 regulates the repair of UVB-induced DNA damage and tumorigenicity.Toxicology and applied pharmacology · 2023Article
- Acetyl-CoA biosynthesis drives resistance to histone acetyltransferase inhibition.Nature chemical biology · 2023Article
- Chemoproteomics Yields a Selective Molecular Host for Acetyl-CoA.Journal of the American Chemical Society · 2023Article
- Acetyl-CoA metabolism in cancer.Nature reviews. Cancer · 2023Review
- N-acetyltransferase 10 promotes colon cancer progression by inhibiting ferroptosis through N4-acetylation and stabilization of ferroptosis suppressor protein 1 (FSP1) mRNA.Cancer communications (London, England) · 2022Article
- Merits of Diazirine Photo-Immobilization for Target Profiling of Natural Products and Cofactors.ACS chemical biology · 2022Article
- Investigating Peptide-Coenzyme A Conjugates as Chemical Probes for Proteomic Profiling of N-Terminal and Lysine Acetyltransferases.Chembiochem : a European journal of chemical biology · 2022Article
- Poly(ADP-ribosyl)ation of acetyltransferase NAT10 by PARP1 is required for its nucleoplasmic translocation and function in response to DNA damage.Cell communication and signaling : CCS · 2022Article
- Functionalised Cofactor Mimics for Interactome Discovery and Beyond.Angewandte Chemie (International ed. in English) · 2022Review
- NAT10-mediated mRNA N4-acetylcytidine modification promotes bladder cancer progression.Clinical and translational medicine · 2022Article
- Remodelin Is a Cryptic Assay Interference Chemotype That Does Not Inhibit NAT10-Dependent Cytidine Acetylation.ACS medicinal chemistry letters · 2021Article
- Harnessing Ionic Selectivity in Acetyltransferase Chemoproteomic Probes.ACS chemical biology · 2021Article
- Characterization of SpecificACS medicinal chemistry letters · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Lysine acetyltransferases (KATs) are key mediators of cell signaling. Methods capable of providing new insights into their regulation thus constitute an important goal. Here we report an optimized platform for profiling KAT-ligand interactions in complex proteomes using inhibitor-functionalized capture resins. This approach greatly expands the scope of KATs, KAT complexes, and CoA-dependent enzymes accessible to chemoproteomic methods. This enhanced profiling platform is then applied in the most comprehensive analysis to date of KAT inhibition by the feedback metabolite CoA. Our studies reveal that members of the KAT superfamily possess a spectrum of sensitivity to CoA and highlight NAT10 as a novel KAT that may be susceptible to metabolic feedback inhibition. This platform provides a powerful tool to define the potency and selectivity of reversible stimuli, such as small molecules and metabolites, that regulate KAT-dependent signaling.
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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.