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@ARTICLE{Witte:38434,
      author       = {Witte, V. and Laffert, B. and Rosorius, O. and Lischka, P.
                      and Blume, K. and Galler, G. and Stilper, A. and Willbold,
                      D. and Blume, K. and D'Aloja, P. and Sixt, M. and Kolanus,
                      J. and Ott, M. and Kolanus, W. and Schuler, G. and Baur, A.
                      S.},
      title        = {{HIV}-1 {N}ef {M}imics an {I}ntgrin {R}eceptor {S}ignal
                      that {R}ecruits the {P}olycomb {G}roup {P}rotein {E}ed to
                      the {P}lasma {M}embrane},
      journal      = {Molecular cell},
      volume       = {13},
      issn         = {1097-2765},
      address      = {[Cambridge, Mass.]},
      publisher    = {Cell Press},
      reportid     = {PreJuSER-38434},
      pages        = {179 - 190},
      year         = {2004},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {The Nef protein of human and simian immunodeficiency virus
                      (HIV/SIV) is believed to interfere with T cell activation
                      signals by forming a signaling complex at the plasma
                      membrane. Composition and function of the complex are not
                      fully understood. Here we report that Nef recruits the
                      Polycomb Group (PcG) protein Eed, so far known as a nuclear
                      factor and repressor of transcription, to the membrane of
                      cells. The Nef-induced translocation of Eed led to a potent
                      stimulation of Tat-dependent HIV transcription, implying
                      that Eed removal from the nucleus is required for optimal
                      Tat function. Similar to Nef action, activation of integrin
                      receptors recruited Eed to the plasma membrane, also leading
                      to enhanced Tat/Nef-mediated transcription. Our results
                      suggest a link between membrane-associated activation
                      processes and transcriptional derepression and demonstrate
                      how HIV exploits this mechanism.},
      keywords     = {J (WoSType)},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)VDB58},
      pnm          = {Neurowissenschaften},
      pid          = {G:(DE-Juel1)FUEK255},
      shelfmark    = {Biochemistry $\&$ Molecular Biology / Cell Biology},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000188797700003},
      doi          = {10.1016/S1097-2765(04)00004-8},
      url          = {https://juser.fz-juelich.de/record/38434},
}