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@ARTICLE{Zhou:124426,
      author       = {C. Zhou and E. Martinez and D. Di Marcantonio and N.
                      Solanki-Patel and T. Aghayev and S. Peri and F. Ferraro and
                      T. Skorski and C. Scholl$^*$ and S. Fröhling$^*$ and S.
                      Balachandran and D. L. Wiest and S. M. Sykes},
      title        = {{JUN} is a key transcriptional regulator of the unfolded
                      protein response in acute myeloid leukemia.},
      journal      = {Leukemia},
      volume       = {31},
      number       = {5},
      issn         = {1476-5551},
      address      = {Basingstoke},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-01303},
      pages        = {1196 - 1205},
      year         = {2017},
      abstract     = {The transcription factor JUN is frequently overexpressed in
                      multiple genetic subtypes of acute myeloid leukemia (AML);
                      however, the functional role of JUN in AML is not well
                      defined. Here we report that short hairpin RNA
                      (shRNA)-mediated inhibition of JUN decreases AML cell
                      survival and propagation in vivo. By performing RNA
                      sequencing analysis, we discovered that JUN inhibition
                      reduces the transcriptional output of the unfolded protein
                      response (UPR), an intracellular signaling transduction
                      network activated by endoplasmic reticulum (ER) stress.
                      Specifically, we found that JUN is activated by MEK
                      signaling in response to ER stress, and that JUN binds to
                      the promoters of several key UPR effectors, such as XBP1 and
                      ATF4, to activate their transcription and allow AML cells to
                      properly negotiate ER stress. In addition, we observed that
                      shRNA-mediated inhibition of XBP1 or ATF4 induces AML cell
                      apoptosis and significantly extends disease latency in vivo
                      tying the reduced survival mediated by JUN inhibition to the
                      loss of pro-survival UPR signaling. These data uncover a
                      previously unrecognized role of JUN as a regulator of the
                      UPR as well as provide key new insights into the how ER
                      stress responses contribute to AML and identify JUN and the
                      UPR as promising therapeutic targets in this disease.},
      cin          = {G100 / G102},
      ddc          = {610},
      cid          = {I:(DE-He78)G100-20160331 / I:(DE-He78)G102-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27840425},
      doi          = {10.1038/leu.2016.329},
      url          = {https://inrepo02.dkfz.de/record/124426},
}