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@PHDTHESIS{Martincuks:684539,
      author       = {Martincuks, Antons},
      othercontributors = {Müller-Newen, Gerhard and Zenke, Martin and Lüscher,
                          Bernhard},
      title        = {{R}ole of {STAT}3 {N}-terminal domain and {GAS}-site
                      recognition in signaling and crosstalk with {STAT}1 and
                      {NF}-κ{B}},
      school       = {RWTH Aachen University},
      type         = {Dissertation},
      address      = {Aachen},
      reportid     = {RWTH-2017-01944},
      pages        = {1 Online-Ressource (171 Seiten) : Illustrationen,
                      Diagramme},
      year         = {2017},
      note         = {Veröffentlicht auf dem Publikationsserver der RWTH Aachen
                      University; Dissertation, RWTH Aachen University, 2017},
      abstract     = {Signal transducer and activator of transcription 3 (STAT3)
                      is a ubiquitous transcription factor involved in many
                      biological processes, including hematopoiesis, development
                      and immune response. Dysfunctional STAT3 signalling has been
                      reported in many pathophysiological conditions such cancer,
                      chronic inflammation and fibrosis. In the first part of this
                      work, we investigated the functions of the N-terminal domain
                      and GAS-site recognition during IL-6-induced STAT3
                      signaling. Our results demonstrate the nonessential role of
                      GAS-element recognition for both cytokine-induced and basal
                      nuclear import of STAT3. In turn, deletion of the NTD
                      markedly decreased nuclear accumulation upon IL-6 treatment
                      resulting in a prolonged accumulation of phosphorylated
                      dimers in the cytoplasm, at the same time preserving
                      specific DNA recognition ability of the truncation mutant.
                      Observed defect in nuclear localization could not be
                      explained by flawed importin-α binding. Furthermore, our
                      data indicated mechanistic differences between active and
                      latent nuclear trafficking of STAT3, as well as between
                      STAT1 and STAT3 active nuclear import.In the second part of
                      this thesis, we analyzed the excessive STAT1 activation in
                      STAT3-deficient cells upon IL-6 treatment. Our findings show
                      that STAT3-mediated regulation of IL-6-induced STAT1
                      signaling depends on STAT3 target gene expression, but not
                      on isolated STAT3 NTD functions. In the third part, we
                      demonstrated that NF-κB and STAT3 have no direct influence
                      on each other canonical signaling pathways. Instead, the
                      expression of NF-κB subunit p65 correlates with total
                      levels of STAT1 and STAT3.In the final part of this work, we
                      characterized a STAT3-YFP knock-in murine model as a
                      potentially powerful tool for the visualization of STAT3 in
                      vivo. Our data show that STAT3-YFP Knock-In mice have been
                      successfully generated and that the YFP fluorescence can be
                      detected by common microscopy techniques. The STAT3-YFP
                      knock-in mice will be a valuable tool for deciphering the
                      function of STAT3 in vivo.},
      cin          = {513000-2 / 811002-2 / 160000},
      ddc          = {570},
      cid          = {$I:(DE-82)513000-2_20140620$ / $I:(DE-82)811002-2_20140620$
                      / $I:(DE-82)160000_20140620$},
      typ          = {PUB:(DE-HGF)11},
      urn          = {urn:nbn:de:hbz:82-rwth-2017-019446},
      doi          = {10.18154/RWTH-2017-01944},
      url          = {https://publications.rwth-aachen.de/record/684539},
}