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Thomas Sauer
Researcher at University of Vienna
Publications - 7
Citations - 1013
Thomas Sauer is an academic researcher from University of Vienna. The author has contributed to research in topics: Cell cycle & Lipofectamine. The author has an hindex of 7, co-authored 7 publications receiving 975 citations. Previous affiliations of Thomas Sauer include Max F. Perutz Laboratories.
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Cell cycle dependence of gene transfer by lipoplex, polyplex and recombinant adenovirus
TL;DR: The results indicate that mitotic activity enhances transfections not only by lipoplexes but also by polyplexes, but not a viral system which has an efficient nuclear entry machinery, suggesting that transfection close to M phase is facilitated perhaps by nuclear membrane breakdown.
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Overcoming the Nuclear Barrier: Cell Cycle Independent Nonviral Gene Transfer with Linear Polyethylenimine or Electroporation
TL;DR: It is suggested that DNA electroporation and DNA transfection with linear PEI particles have improved nuclear import characteristics relative to the other tested DNA delivery systems.
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Evidence for a size-sensing mechanism in animal cells
TL;DR: Evidence is provided that vertebrate cells can respond to cell size alterations (induced either through different growth factor signalling or DNA synthesis inhibitors) by compensatory shortening of the subsequent G1 phase, suggesting that an active size threshold mechanism exists in G1, which induces adjustment of cell-cycle length in the next cycle, thus ensuring maintenance of a proper balance between growth and proliferation rates in vertebrates.
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Overexpression of Thymidine Kinase mRNA Eliminates Cell Cycle Regulation of Thymidine Kinase Enzyme Activity
TL;DR: Data indicate that post-transcriptional regulation of TK is tightly coupled to the amount of mRNA; high concentrations apparently titrate a factor(s) required for repressing TK production during G and presumably also G.
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Structure and function of the iron-responsive element from human ferritin l chain mrna
TL;DR: The cis-acting regulatory IRE motif of human ferritin L chain mRNA was capable of repressing translation under iron deprivation but permitted mobilization of the transcripts into polysomes following iron repletion in vivo.