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Svein Isungset Støve

Postdoktor
  • E-postSvein.Stove@uib.no
  • Telefon+47 55 58 43 49
  • Besøksadresse
    Jonas Lies vei 91
  • Postadresse
    Postboks 7804
    5020 Bergen
Vitenskapelig artikkel
  • 2019. Characterization of Evolutionarily Conserved Trypanosoma cruzi NatC and NatA-N-Terminal Acetyltransferase Complexes. Journal of Parasitology Research.
  • 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.
  • 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.
  • 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.
  • 2018. A novel NAA10 variant with impaired acetyltransferase activity causes developmental delay, intellectual disability, and hypertrophic cardiomyopathy. European Journal of Human Genetics. 1-12.
  • 2016. Expanding the phenotype associated with NAA10-related N-terminal acetylation deficiency. Human Mutation. 755-764.
  • 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.
  • 2015. NAA10 mutation causing a novel intellectual disability syndrome with Long QT due to N-terminal acetyltransferase impairment. Scientific Reports.
  • 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.
  • 2015. Biochemical and cellular analysis of Ogden syndrome reveals downstream Nt-acetylation defects. Human Molecular Genetics. 1956-1976.
  • 2015. An organellar Nα-acetyltransferase, Naa60, acetylates cytosolic n termini of transmembrane proteins and maintains golgi integrity. Cell reports. 1362-1374.
  • 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.
  • 2013. Protein N-terminal acetyltransferases act as N-terminal propionyltransferases in vitro and in vivo. Molecular & Cellular Proteomics. 42-54.
Vitenskapelig foredrag
  • 2019. Biophysical studies of a protein complex involved in dopamine synthesis and vesicular packing .
  • 2014. N-terminal acetylation and the Ogden syndrome.
  • 2012. The Ogden Syndrome.
Leder
  • 2015. Naa10 in development and disease. OncoTarget. 34041-34042.
Doktorgradsavhandling
  • 2015. Functional analysis of Na-acetyltransferase 10(NAA10) variants identified in patients with genetic disorders.
Poster
  • 2018. naa10 knockdown and NatA inhibition point to role for the NatA complex in zebrafish dorsoventral axis formation .
  • 2018. Regulation of protein-protein interactions crucial for dopamine synthesis.
  • 2018. Inhibition of the Actin N-terminal acetyltransferase NAA80.
  • 2015. NAA10 missense mutations cause neurodevelopmental delay in eight female patients.
  • 2014. In silico, in vitro and in vivo models reveal functional impairment of the Ogden syndrome N-terminal acetyltransferase Naa10 S37P mutant.
  • 2012. Structural modeling and kinetic studies of a mutant N-terminal acetyltransferase, hNaa10p Ser37Pro, causing an infantile lethal disorder.
  • 2012. An x-linked infantile lethal disorder caused by N-terminal acetyltransferase deficiency.
  • 2012. An X-linked infantile lethal disease, the Ogden syndrome, and the functional implications of the hNaa10p S37P mutation.

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