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Anna Karlsson
Researcher at Karolinska University Hospital
Publications - 170
Citations - 6291
Anna Karlsson is an academic researcher from Karolinska University Hospital. The author has contributed to research in topics: Kinase & Thymidine kinase. The author has an hindex of 43, co-authored 168 publications receiving 5981 citations. Previous affiliations of Anna Karlsson include Pasteur Institute & Max Planck Society.
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1,2,3-Triazole-[2',5'-bis-O-(tert-butyldimethylsilyl)-beta-D- ribofuranosyl]-3'-spiro-5"-(4"-amino-1",2"-oxathiole 2",2"-dioxide) (TSAO) analogues: synthesis and anti-HIV-1 activity.
Rosa Alvarez,Sonsoles Velázquez,Ana San-Félix,Stefano Aquaro,Erik De Clercq,Carlo Federico Perno,Anna Karlsson,Jan Balzarini,María-José Camarasa +8 more
TL;DR: Several 4- or 5-monosubsituted and 4,5-disubstituted 1,2,3-triazole analogues of the anti-HIV-1 lead compound TSAO have been prepared and evaluated as inhibitors of HIV-1-induced cytopathicity.
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Phosphorylation of nucleosides and nucleoside analogs by mammalian nucleoside monophosphate kinases
TL;DR: This overview is focused on the substrate specificity, tissue distribution, and subcellular location of the mammalian monophosphate kinases and their role in the activation of nucleoside and nucleotide analogs.
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Identification and characterization of SarH1, a new global regulator of virulence gene expression in Staphylococcus aureus
TL;DR: It is shown that both the agr‐dependent suppression of protein A production and the sarA‐dependent stimulation of alpha‐toxin production is mediated via a new regulator, SarH1, which belongs to a family of Sar homologues.
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Decreased Amounts of Cell Wall-Associated Protein A and Fibronectin-Binding Proteins in Staphylococcus aureus sarA Mutants due to Up-Regulation of Extracellular Proteases
TL;DR: It can be concluded that the serine protease is the most important protease in the release of cell-bound FnBPs and protein A, which requires aureolysin to be activated.
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HIV-1-specific reverse transcriptase inhibitors show differential activity against HIV-1 mutant strains containing different amino acid substitutions in the reverse transcriptase.
Jan Balzarini,Anna Karlsson,María-Jesús Pérez-Pérez,Lotta Vrang,Johan Walbers,Hong Zhang,Bo Öberg,Anne-Mieke Vandamme,María-José Camarasa,Erik De Clercq +9 more
TL;DR: Serial passage of HIV-1 in CEM or MT-4 cell cultures in the presence of different HIV- 1-specific reverse transcriptase (RT) inhibitors yielded mutant viruses which were resistant (i.e., 200- to 1000-fold less sensitive) to the homologous compounds.