@phdthesis{Czech2013,
  author    = {Czech, Andreas},
  title     = {Variations in the tRNA pool of mammalian cells upon differentiation and oxidative stress},
  address   = {Potsdam},
  pages     = {98 S.},
  year      = {2013},
  language  = {en}
}
@article{CzechWendeMoerletal.2013,
  author    = {Czech, Andreas and Wende, Sandra and Moerl, Mario and Pan, Tao and Ignatova, Zoya},
  title     = {Reversible and rapid transfer-RNA deactivation as a mechanism of translational repression in stress},
  series = {PLoS Genetics : a peer-reviewed, open-access journal},
  volume    = {9},
  journal   = {PLoS Genetics : a peer-reviewed, open-access journal},
  number    = {8},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1553-7404},
  doi       = {10.1371/journal.pgen.1003767},
  pages     = {9},
  year      = {2013},
  abstract  = {Stress-induced changes of gene expression are crucial for survival of eukaryotic cells. Regulation at the level of translation provides the necessary plasticity for immediate changes of cellular activities and protein levels. In this study, we demonstrate that exposure to oxidative stress results in a quick repression of translation by deactivation of the aminoacylends of all transfer-RNA (tRNA). An oxidative-stress activated nuclease, angiogenin, cleaves first within the conserved single-stranded 3'-CCA termini of all tRNAs, thereby blocking their use in translation. This CCA deactivation is reversible and quickly repairable by the CCA-adding enzyme [ATP(CTP): tRNA nucleotidyltransferase]. Through this mechanism the eukaryotic cell dynamically represses and reactivates translation at low metabolic costs.},
  language  = {en}
}
@article{GirstmairSaffertRodeetal.2013,
  author    = {Girstmair, Hannah and Saffert, Paul and Rode, Sascha and Czech, Andreas and Holland, Gudrun and Bannert, Norbert and Ignatova, Zoya},
  title     = {Depletion of Cognate Charged Transfer RNA Causes Translational Frameshifting within the Expanded CAG Stretch in Huntingtin},
  series = {Cell reports},
  volume    = {3},
  journal   = {Cell reports},
  number    = {1},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {2211-1247},
  doi       = {10.1016/j.celrep.2012.12.019},
  pages     = {148 -- 159},
  year      = {2013},
  abstract  = {Huntington disease (HD), a dominantly inherited neurodegenerative disorder caused by the expansion of a CAG-encoded polyglutamine (polyQ) repeat in huntingtin (Htt), displays a highly heterogeneous etiopathology and disease onset. Here, we show that the translation of expanded CAG repeats in mutant Htt exon 1 leads to a depletion of charged glutaminyl-transfer RNA (tRNA) Gln-CUG that pairs exclusively to the CAG codon. This results in translational frameshifting and the generation of various transframe-encoded species that differently modulate the conformational switch to nucleate fibrillization of the parental polyQ protein. Intriguingly, the frameshifting frequency varies strongly among different cell lines and is higher in cells with intrinsically lower concentrations of tRNA Gln-CUG. The concentration of tRNA Gln-CUG also differs among different brain areas in the mouse. We propose that translational frameshifting may act as a significant disease modifier that contributes to the cell-selective neurotoxicity and disease course heterogeneity of HD on both cellular and individual levels.},
  language  = {en}
}