@article{VučićevićGehreDhamijaetal.2016,
  author    = {Vučićević, Dubravka and Gehre, Maja and Dhamija, Sonam and Friis-Hansen, Lennart and Meierhofer, David and Sauer, Sascha and {\O}rom, Ulf Andersson},
  title     = {The long non-coding RNA PARROT is an upstream regulator of c-Myc and affects proliferation and translation},
  series = {Oncotarget},
  volume    = {7},
  journal   = {Oncotarget},
  number    = {23},
  doi       = {10.18632/oncotarget.8985},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-166519},
  pages     = {33934-33947},
  year      = {2016},
  abstract  = {Long non-coding RNAs are important regulators of gene expression and signaling pathways. The expression of long ncRNAs is dysregulated in cancer and other diseases. The identification and characterization of long ncRNAs is often challenging due to their low expression level and localization to chromatin. Here, we identify a functional long ncRNA, PARROT (Proliferation Associated RNA and Regulator Of Translation) transcribed by RNA polymerase II and expressed at a relatively high level in a number of cell lines. The PARROT long ncRNA is associated with proliferation in both transformed and normal cell lines. We characterize the long ncRNA PARROT as an upstream regulator of c-Myc affecting cellular proliferation and translation using RNA sequencing and mass spectrometry following depletion of the long ncRNA. PARROT is repressed during senescence of human mammary epithelial cells and overexpressed in some cancers, suggesting an important association with proliferation through regulation of c-Myc. With this study, we add to the knowledge of cytoplasmic functional long ncRNAs and extent the long ncRNA-Myc regulatory network in transformed and normal cells.},
  language  = {en}
}
@article{ScognamiglioCabezasWallscheidThieretal.2016,
  author    = {Scognamiglio, Roberta and Cabezas-Wallscheid, Nina and Thier, Marc Christian and Altamura, Sandro and Reyes, Alejandro and Prendergast, {\´A}ine M. and Baumg{\"a}rtner, Daniel and Carnevalli, Larissa S. and Atzberger, Ann and Haas, Simon and von Paleske, Lisa and Boroviak, Thorsten and W{\"o}rsd{\"o}rfer, Philipp and Essers, Marieke A. G. and Kloz, Ulrich and Eisenman, Robert N. and Edenhofer, Frank and Bertone, Paul and Huber, Wolfgang and van der Hoeven, Franciscus and Smith, Austin and Trumpp, Andreas},
  title     = {Myc depletion induces a pluripotent dormant state mimicking diapause},
  series = {Cell},
  volume    = {164},
  journal   = {Cell},
  number    = {4},
  doi       = {10.1016/j.cell.2015.12.033},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-190868},
  pages     = {668-680},
  year      = {2016},
  abstract  = {Mouse embryonic stem cells (ESCs) are maintained in a naive ground state of pluripotency in the presence of MEK and GSK3 inhibitors. Here, we show that ground-state ESCs express low Myc levels. Deletion of both c-myc and N-myc (dKO) or pharmacological inhibition of Myc activity strongly decreases transcription, splicing, and protein synthesis, leading to proliferation arrest. This process is reversible and occurs without affecting pluripotency, suggesting that Myc-depleted stem cells enter a state of dormancy similar to embryonic diapause. Indeed, c-Myc is depleted in diapaused blastocysts, and the differential expression signatures of dKO ESCs and diapaused epiblasts are remarkably similar. Following Myc inhibition, pre-implantation blastocysts enter biosynthetic dormancy but can progress through their normal developmental program after transfer into pseudo-pregnant recipients. Our study shows that Myc controls the biosynthetic machinery of stem cells without affecting their potency, thus regulating their entry and exit from the dormant state.},
  language  = {en}
}