Svein Isungset Støve's picture

Svein Isungset Støve

  • E-mailsvein.stove@uib.no
  • Visitor Address
    Jonas Lies vei 91
    5009 Bergen
  • Postal Address
    Postboks 7804
    5020 Bergen
Academic article
  • Show author(s) (2023). Optimized bisubstrate inhibitors for the actin N-terminal acetyltransferase NAA80. Frontiers in Chemistry.
  • Show author(s) (2022). Inhibition of VMAT2 by β2-adrenergic agonists, antagonists, and the atypical antipsychotic ziprasidone. Communications Biology. 1-14.
  • Show author(s) (2019). Characterization of Evolutionarily Conserved Trypanosoma cruzi NatC and NatA-N-Terminal Acetyltransferase Complexes. Journal of Parasitology Research.
  • Show author(s) (2019). A scavenger receptor B (CD36)-like protein is a potential mediator of intestinal heme absorption in the hematophagous ectoparasite Lepeophtheirus salmonis. Scientific Reports. 1-14.
  • Show author(s) (2018). Structural determinants and cellular environment define processed actin as the sole substrate of the N-terminal acetyltransferase NAA80. Proceedings of the National Academy of Sciences of the United States of America. 4405-4410.
  • Show author(s) (2018). NAA10 dysfunction with normal NatA-complex activity in a girl with non-syndromic ID and a de novo NAA10 p.(V111G) variant - a case report. BMC Medical Genetics. 1-9.
  • Show author(s) (2018). A novel NAA10 variant with impaired acetyltransferase activity causes developmental delay, intellectual disability, and hypertrophic cardiomyopathy. European Journal of Human Genetics. 1-12.
  • Show author(s) (2016). Expanding the phenotype associated with NAA10-related N-terminal acetylation deficiency. Human Mutation. 755-764.
  • Show author(s) (2016). Crystal structure of the Golgi-associated human N-alpha acetyltransferase 60 (Naa60/NatF) reveals the molecular determinants for substrate-specific acetylation. Structure. 1044-1056.
  • Show author(s) (2015). NAA10 mutation causing a novel intellectual disability syndrome with Long QT due to N-terminal acetyltransferase impairment. Scientific Reports.
  • Show author(s) (2015). De novo missense mutations in the NAA10 gene cause severe non-syndromic developmental delay in males and females. European Journal of Human Genetics. 602-609.
  • Show author(s) (2015). Biochemical and cellular analysis of Ogden syndrome reveals downstream Nt-acetylation defects. Human Molecular Genetics. 1956-1976.
  • Show author(s) (2015). An organellar Nα-acetyltransferase, Naa60, acetylates cytosolic n termini of transmembrane proteins and maintains golgi integrity. Cell reports. 1362-1374.
  • Show author(s) (2014). A Saccharomyces cerevisiae model reveals in vivo functional impairment of the Ogden syndrome N-terminal acetyltransferase NAA10 Ser37Pro mutant. Molecular & Cellular Proteomics. 2031-2041.
  • Show author(s) (2013). Protein N-terminal acetyltransferases act as N-terminal propionyltransferases in vitro and in vivo. Molecular & Cellular Proteomics. 42-54.
Academic lecture
  • Show author(s) (2022). High-throughput screening for VMAT2 activity modulators.
  • Show author(s) (2022). High-throughput screening approaches for vesicular monoamine transporter 2 and mitochondrial complex I.
  • Show author(s) (2019). Biophysical studies of a protein complex involved in dopamine synthesis and vesicular packing .
  • Show author(s) (2014). N-terminal acetylation and the Ogden syndrome.
  • Show author(s) (2012). The Ogden Syndrome.
  • Show author(s) (2015). Naa10 in development and disease. OncoTarget. 34041-34042.
Masters thesis
  • Show author(s) (2023). Towards the therapeutic correction of mitochondrial Complex I deficiency in dopaminergic cell models.
  • Show author(s) (2023). Screening for VMAT2 chaperones and activity modulators.
Doctoral dissertation
  • Show author(s) (2015). Functional analysis of Na-acetyltransferase 10(NAA10) variants identified in patients with genetic disorders.
  • Show author(s) (2022). Screening for modulators of vesicular monoamine transporter 2 activity in transfected Hek293 cells using a fluorescent substrate.
  • Show author(s) (2022). High-throughput screening for VMAT2 activity modulators.
  • Show author(s) (2022). Does alpha-Synuclein modulate Tyrosine Hydoxylase activity?
  • Show author(s) (2020). Searching for new inhibitors of vesicular monoamine transporter 2 by differential scanning fluorimetry.
  • Show author(s) (2020). Phosphorylated TH hinges with vesicular membrane proteins for axonal transport.
  • Show author(s) (2020). Inhibition of the Actin N-terminal acetyltransferase NAA80.
  • Show author(s) (2020). Identification of VMAT2 inhibitory compounds.
  • Show author(s) (2020). Comparing detergent micelles and polymer nanodiscs for solubilization and purification of the integral membrane protein vesicular monoamine transporter 2.
  • Show author(s) (2018). naa10 knockdown and NatA inhibition point to role for the NatA complex in zebrafish dorsoventral axis formation .
  • Show author(s) (2018). Regulation of protein-protein interactions crucial for dopamine synthesis.
  • Show author(s) (2018). Inhibition of the Actin N-terminal acetyltransferase NAA80.
  • Show author(s) (2015). NAA10 missense mutations cause neurodevelopmental delay in eight female patients.
  • Show author(s) (2014). In silico, in vitro and in vivo models reveal functional impairment of the Ogden syndrome N-terminal acetyltransferase Naa10 S37P mutant.
  • Show author(s) (2012). Structural modeling and kinetic studies of a mutant N-terminal acetyltransferase, hNaa10p Ser37Pro, causing an infantile lethal disorder.
  • Show author(s) (2012). An x-linked infantile lethal disorder caused by N-terminal acetyltransferase deficiency.
  • Show author(s) (2012). An X-linked infantile lethal disease, the Ogden syndrome, and the functional implications of the hNaa10p S37P mutation.
  • Show author(s) (2020). Differential scanning fluorimetry in the screening and validation of pharmacological chaperones for soluble and membrane proteins. 329-343. In:
    • Show author(s) (2020). Protein Homeostasis Diseases: Mechanisms and Novel Therapies. Elsevier.

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