ArticleBioscience reports2017
Depletion of the human N-terminal acetyltransferase hNaa30 disrupts Golgi integrity and ARFRP1 localization.
Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Investigating the Shared Genetic Architecture Between Leukocyte Telomere Length and Prostate Cancer.The world journal of men's health · 2025Article
- N-terminal acetylation shields proteins from degradation and promotes age-dependent motility and longevity.Nature communications · 2023Article
- Molecular role of NAA38 in thermostability and catalytic activity of the human NatC N-terminal acetyltransferase.Structure (London, England : 1993) · 2023Article
- Targeted Proteomic Analysis of Small GTPases in Radioresistant Breast Cancer Cells.Analytical chemistry · 2022Article
- Chemogenetic profiling reveals PP2A-independent cytotoxicity of proposed PP2A activators iHAP1 and DT-061.The EMBO journal · 2022Article
- Divergent architecture of the heterotrimeric NatC complex explains N-terminal acetylation of cognate substrates.Nature communications · 2020Article
- Spotlight on protein N-terminal acetylation.Experimental & molecular medicine · 2018Review
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4 authors at 3 institutions in 1 country.
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Abstract
The organization of the Golgi apparatus (GA) is tightly regulated. Golgi stack scattering is observed in cellular processes such as apoptosis and mitosis, and has also been associated with disruption of cellular lipid metabolism and neurodegenerative diseases. Our studies show that depletion of the human N-α-acetyltransferase 30 (hNaa30) induces fragmentation of the Golgi stack in HeLa and CAL-62 cell lines. The GA associated GTPase ADP ribosylation factor related protein 1 (ARFRP1) was previously shown to require N-terminal acetylation for membrane association and based on its N-terminal sequence, it is likely to be a substrate of hNaa30. ARFRP1 is involved in endosome-to-
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