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@ARTICLE{Fearnley:119924,
      author       = {G. W. Fearnley and A. F. Odell and A. M. Latham and N. A.
                      Mughal and A. F. Bruns and N. J. Burgoyne and S.
                      Homer-Vanniasinkam and I. C. Zachary and M. Hollstein$^*$
                      and S. B. Wheatcroft and S. Ponnambalam},
      title        = {{VEGF}-{A} isoforms differentially regulate
                      {ATF}-2-dependent {VCAM}-1 gene expression and
                      endothelial-leukocyte interactions.},
      journal      = {Molecular biology of the cell},
      volume       = {25},
      number       = {16},
      issn         = {1059-1524},
      address      = {Bethesda, Md.},
      publisher    = {American Society for Cell Biology},
      reportid     = {DKFZ-2017-00515},
      pages        = {2509 - 2521},
      year         = {2014},
      abstract     = {Vascular endothelial growth factor A (VEGF-A) regulates
                      many aspects of vascular physiology. VEGF-A stimulates
                      signal transduction pathways that modulate endothelial
                      outputs such as cell migration, proliferation,
                      tubulogenesis, and cell-cell interactions. Multiple VEGF-A
                      isoforms exist, but the biological significance of this is
                      unclear. Here we analyzed VEGF-A isoform-specific
                      stimulation of VCAM-1 gene expression, which controls
                      endothelial-leukocyte interactions, and show that this is
                      dependent on both ERK1/2 and activating transcription
                      factor-2 (ATF-2). VEGF-A isoforms showed differential ERK1/2
                      and p38 MAPK phosphorylation kinetics. A key feature of
                      VEGF-A isoform-specific ERK1/2 activation and nuclear
                      translocation was increased phosphorylation of ATF-2 on
                      threonine residue 71 (T71). Using reverse genetics, we
                      showed ATF-2 to be functionally required for
                      VEGF-A-stimulated endothelial VCAM-1 gene expression. ATF-2
                      knockdown blocked VEGF-A-stimulated VCAM-1 expression and
                      endothelial-leukocyte interactions. ATF-2 was also required
                      for other endothelial cell outputs, such as cell migration
                      and tubulogenesis. In contrast, VCAM-1 was essential only
                      for promoting endothelial-leukocyte interactions. This work
                      presents a new paradigm for understanding how soluble growth
                      factor isoforms program complex cellular outputs and
                      responses by modulating signal transduction pathways.},
      keywords     = {ATF2 protein, human (NLM Chemicals) / Activating
                      Transcription Factor 2 (NLM Chemicals) / Protein Isoforms
                      (NLM Chemicals) / VEGFA protein, human (NLM Chemicals) /
                      Vascular Cell Adhesion Molecule-1 (NLM Chemicals) / Vascular
                      Endothelial Growth Factor A (NLM Chemicals) / KDR protein,
                      human (NLM Chemicals) / Vascular Endothelial Growth Factor
                      Receptor-2 (NLM Chemicals)},
      cin          = {C016},
      ddc          = {570},
      cid          = {I:(DE-He78)C016-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24966171},
      pmc          = {pmc:PMC4142621},
      doi          = {10.1091/mbc.E14-05-0962},
      url          = {https://inrepo02.dkfz.de/record/119924},
}