@article{RutkowskiErhardL'Hernaultetal.2015,
  author    = {Rutkowski, Andrzej J. and Erhard, Florian and L'Hernault, Anne and Bonfert, Thomas and Schilhabel, Markus and Crump, Colin and Rosenstiel, Philip and Efstathiou, Stacey and Zimmer, Ralf and Friedel, Caroline C. and D{\"o}lken, Lars},
  title     = {Widespread disruption of host transcription termination in HSV-1 infection},
  series = {Nature Communications},
  volume    = {6},
  journal   = {Nature Communications},
  number    = {7126},
  doi       = {10.1038/ncomms8126},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148643},
  year      = {2015},
  abstract  = {Herpes simplex virus 1 (HSV-1) is an important human pathogen and a paradigm for virus-induced host shut-off. Here we show that global changes in transcription and RNA processing and their impact on translation can be analysed in a single experimental setting by applying 4sU-tagging of newly transcribed RNA and ribosome profiling to lytic HSV-1 infection. Unexpectedly, we find that HSV-1 triggers the disruption of transcription termination of cellular, but not viral, genes. This results in extensive transcription for tens of thousands of nucleotides beyond poly(A) sites and into downstream genes, leading to novel intergenic splicing between exons of neighbouring cellular genes. As a consequence, hundreds of cellular genes seem to be transcriptionally induced but are not translated. In contrast to previous reports, we show that HSV-1 does not inhibit co-transcriptional splicing. Our approach thus substantially advances our understanding of HSV-1 biology and establishes HSV-1 as a model system for studying transcription termination.},
  language  = {en}
}
@article{MurakawaHinzMothesetal.2015,
  author    = {Murakawa, Yasuhiro and Hinz, Michael and Mothes, Janina and Schuetz, Anja and Uhl, Michael and Wyler, Emanuel and Yasuda, Tomoharu and Mastrobuoni, Guido and Friedel, Caroline C. and D{\"o}lken, Lars and Kempa, Stefan and Schmidt-Supprian, Marc and Bl{\"u}thgen, Nils and Backofen, Rolf and Heinemann, Udo and Wolf, Jana and Scheidereit, Claus and Landthaler, Markus},
  title     = {RC3H1 post-transcriptionally regulates A20 mRNA and modulates the activity of the IKK/NF-\(\kappa\)B pathway},
  series = {Nature Communications},
  volume    = {6},
  journal   = {Nature Communications},
  number    = {7367},
  doi       = {10.1038/ncomms8367},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-151596},
  year      = {2015},
  abstract  = {The RNA-binding protein RC3H1 (also known as ROQUIN) promotes TNF\(\alpha\) mRNA decay via a 3'UTR constitutive decay element (CDE). Here we applied PAR-CLIP to human RC3H1 to identify ~3,800 mRNA targets with >16,000 binding sites. A large number of sites are distinct from the consensus CDE and revealed a structure-sequence motif with U-rich sequences embedded in hairpins. RC3H1 binds preferentially short-lived and DNA damage-induced mRNAs, indicating a role of this RNA-binding protein in the post-transcriptional regulation of the DNA damage response. Intriguingly, RC3H1 affects expression of the NF-\(\kappa\)B pathway regulators such as I\(\kappa\)B\(\alpha\) and A20. RC3H1 uses ROQ and Zn-finger domains to contact a binding site in the A20 3'UTR, demonstrating a not yet recognized mode of RC3H1 binding. Knockdown of RC3H1 resulted in increased A20 protein expression, thereby interfering with I\(\kappa\)B kinase and NF-\(\kappa\)B activities, demonstrating that RC3H1 can modulate the activity of the IKK/NF-\(\kappa\)B pathway.},
  language  = {en}
}