ArticleNature communications2020
Molecular basis for N-terminal acetylation by human NatE and its modulation by HYPK.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- HYPK-Related Neurodevelopmental Syndrome: Case Report of Intellectual Disability, Developmental Delay, and Dysmorphic Features.Clinical genetics · 2026Article
- NatA engages in multi-factor complexes at the ribosomal polypeptide tunnel exit.Nature communications · 2026Article
- HYPK promotes N-terminal protein acetylation through rapid ribosome exchange of NatA.Molecular cell · 2025Article
- Mechanistic Insights into Protein Biogenesis and Maturation on the Ribosome.Journal of molecular biology · 2025Review
- Population-scale gene-based analysis of whole-genome sequencing provides insights into metabolic health.Nature genetics · 2025Article
- Illuminating the impact of N-terminal acetylation: from protein to physiology.Nature communications · 2025Review
- Conformational plasticity links structural instability of NAA10Computational and structural biotechnology journal · 2024Article
- Multi-protein assemblies orchestrate co-translational enzymatic processing on the human ribosome.Nature communications · 2024Article
- Article
- Acetyltransferase in cardiovascular disease and aging.The journal of cardiovascular aging · 2024Article
- Impact of Protein NLife (Basel, Switzerland) · 2023Review
- Molecular role of NAA38 in thermostability and catalytic activity of the human NatC N-terminal acetyltransferase.Structure (London, England : 1993) · 2023Article
- NAA60 (HAT4): the newly discovered bi-functional Golgi member of the acetyltransferase family.Clinical epigenetics · 2022Review
- From Nucleus to Membrane: A Subcellular Map of the N-Acetylation Machinery in Plants.International journal of molecular sciences · 2022Review
- Extended N-Terminal Acetyltransferase Naa50 in Filamentous Fungi Adds to Naa50 Diversity.International journal of molecular sciences · 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
- HYPK promotes the activity of theScience advances · 2022Article
- Possible Catch-Up Developmental Trajectories for Children with Mild Developmental Delay Caused byGenes · 2022Review
- Pan-cancer analysis reveals NAA50 as a cancer prognosis and immune infiltration-related biomarker.Frontiers in genetics · 2022Article
- Hydroxylation of the Acetyltransferase NAA10 Trp38 Is Not an Enzyme-Switch in Human Cells.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The human N-terminal acetyltransferase E (NatE) contains NAA10 and NAA50 catalytic, and NAA15 auxiliary subunits and associates with HYPK, a protein with intrinsic NAA10 inhibitory activity. NatE co-translationally acetylates the N-terminus of half the proteome to mediate diverse biological processes, including protein half-life, localization, and interaction. The molecular basis for how NatE and HYPK cooperate is unknown. Here, we report the cryo-EM structures of human NatE and NatE/HYPK complexes and associated biochemistry. We reveal that NAA50 and HYPK exhibit negative cooperative binding to NAA15 in vitro and in human cells by inducing NAA15 shifts in opposing directions. NAA50 and HYPK each contribute to NAA10 activity inhibition through structural alteration of the NAA10 substrate-binding site. NAA50 activity is increased through NAA15 tethering, but is inhibited by HYPK through structural alteration of the NatE substrate-binding site. These studies reveal the molecular basis for coordinated N-terminal acetylation by NatE and HYPK.
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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.