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@ARTICLE{Scognamiglio:130534,
      author       = {R. Scognamiglio$^*$ and N. Cabezas-Wallscheid$^*$ and M.
                      Thier$^*$ and S. Altamura and A. Reyes and A.
                      Prendergast$^*$ and D. Baumgärtner$^*$ and L. S.
                      Carnevalli$^*$ and A. Atzberger and S. Haas$^*$ and L. von
                      Paleske$^*$ and T. Boroviak and P. Wörsdörfer and M.
                      Essers$^*$ and U. Kloz$^*$ and R. N. Eisenman and F.
                      Edenhofer and P. Bertone and W. Huber and F. van der
                      Hoeven$^*$ and A. Smith and A. Trumpp$^*$},
      title        = {{M}yc {D}epletion {I}nduces a {P}luripotent {D}ormant
                      {S}tate {M}imicking {D}iapause.},
      journal      = {Cell},
      volume       = {164},
      number       = {4},
      issn         = {0092-8674},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-05613},
      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.},
      keywords     = {Myc protein, mouse (NLM Chemicals) / Proto-Oncogene
                      Proteins c-myc (NLM Chemicals)},
      cin          = {V960 / A010 / A011 / W450 / L101},
      ddc          = {570},
      cid          = {I:(DE-He78)V960-20160331 / I:(DE-He78)A010-20160331 /
                      I:(DE-He78)A011-20160331 / I:(DE-He78)W450-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26871632},
      pmc          = {pmc:PMC4752822},
      doi          = {10.1016/j.cell.2015.12.033},
      url          = {https://inrepo02.dkfz.de/record/130534},
}