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@ARTICLE{Fricke:144710,
      author       = {F. Fricke$^*$ and M. Michalak$^*$ and U. Warnken$^*$ and I.
                      Hausser and M. Schnölzer$^*$ and J. Kopitz$^*$ and J.
                      Gebert$^*$},
      title        = {{SILAC}-{B}ased {Q}uantification of {TGFBR}2-{R}egulated
                      {P}rotein {E}xpression in {E}xtracellular {V}esicles of
                      {M}icrosatellite {U}nstable {C}olorectal {C}ancers.},
      journal      = {International journal of molecular sciences},
      volume       = {20},
      number       = {17},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2019-02152},
      pages        = {4162},
      year         = {2019},
      abstract     = {Microsatellite unstable (MSI) colorectal cancers (CRCs) are
                      characterized by mutational inactivation of Transforming
                      Growth Factor Beta Receptor Type 2 (TGFBR2).
                      TGFBR2-deficient CRCs present altered target gene and
                      protein expression. Such cellular alterations modulate the
                      content of CRC-derived extracellular vesicles (EVs). EVs
                      function as couriers of proteins, nucleic acids, and lipids
                      in intercellular communication. At a qualitative level, we
                      have previously shown that TGFBR2 deficiency causes overall
                      alterations in the EV protein content. To deepen the basic
                      understanding of altered protein dynamics, this work aimed
                      to determine TGFBR2-dependent EV protein signatures in a
                      quantitative manner. Using a stable isotope labeling with
                      amino acids in cell culture (SILAC) approach for mass
                      spectrometry-based quantification, 48 TGFBR2-regulated
                      proteins were identified in MSI CRC-derived EVs. Overall,
                      TGFBR2 deficiency caused upregulation of several EV proteins
                      related to the extracellular matrix and nucleosome as well
                      as downregulation of proteasome-associated proteins. The
                      present study emphasizes the general overlap of proteins
                      between EVs and their parental CRC cells but also highlights
                      the impact of TGFBR2 deficiency on EV protein composition.
                      From a clinical perspective, TGFBR2-regulated quantitative
                      differences of protein expression in EVs might nominate
                      novel biomarkers for liquid biopsy-based MSI typing in the
                      future.},
      cin          = {F210 / B100},
      ddc          = {540},
      cid          = {I:(DE-He78)F210-20160331 / I:(DE-He78)B100-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31454892},
      doi          = {10.3390/ijms20174162},
      url          = {https://inrepo02.dkfz.de/record/144710},
}