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@ARTICLE{Bona:604258,
      author       = {Bona, Alexandra and Seifert, Michael and Thünauer, Roland
                      and Zodel, Kyra and Frew, Ian J. and Römer, Winfried and
                      Walz, Gerd and Yakulov, Toma A.},
      title        = {{MARVEL} domain containing {CMTM}4 affects {CXCR}4
                      trafficking},
      journal      = {Molecular biology of the cell},
      volume       = {33},
      number       = {13},
      issn         = {1059-1524},
      address      = {Bethesda, Md.},
      publisher    = {American Society for Cell Biology},
      reportid     = {PUBDB-2024-01056},
      pages        = {ar116},
      year         = {2022},
      abstract     = {Sections View article Tools ShareAbstractThe MARVEL
                      proteins CMTM4 and CMTM6 control PD-L1, thereby influencing
                      tumor immunity. We found that defective zebrafish cmtm4
                      slowed the development of the posterior lateral line (pLL)
                      by altering the Cxcr4b gradient across the pLL primordium
                      (pLLP). Analysis in mammalian cells uncovered that CMTM4
                      interacted with CXCR4, altering its glycosylation pattern,
                      but did not affect internalization or degradation of CXCR4
                      in the absence of its ligand CXCL12. Synchronized release of
                      CXCR4 from the endoplasmic reticulum revealed that CMTM4
                      slowed CXCR4 trafficking from the endoplasmic reticulum to
                      the plasma membrane without affecting overall cell surface
                      expression. Altered CXCR4 trafficking reduced ligand-induced
                      CXCR4 degradation and affected AKT but not ERK1/2
                      activation. CMTM4 expression, in contrast to that of CXCR4,
                      correlated with the survival of patients with renal cell
                      cancer in the TCGA cohort. Furthermore, we observed that
                      cmtm4 depletion promotes the separation of cells from the
                      pLLP cell cluster in zebrafish embryos. Collectively, our
                      findings indicate that CMTM4 exerts general roles in the
                      biosynthetic pathway of cell surface molecules and seems to
                      affect CXCR4-dependent cell migration.},
      cin          = {CSSB-CF-ALFM},
      ddc          = {570},
      cid          = {I:(DE-H253)CSSB-CF-ALFM-20210629},
      pnm          = {899 - ohne Topic (POF4-899) / DFG project
                      G:(GEPRIS)390939984 - EXC 2189: CIBSS - Centre for
                      Integrative Biological Signalling Studies (390939984) / DFG
                      project G:(GEPRIS)39236281 - EXC 294: BIOSS Zentrum für
                      Biologische Signalstudien - von der Analyse zur Synthese
                      (39236281)},
      pid          = {G:(DE-HGF)POF4-899 / G:(GEPRIS)390939984 /
                      G:(GEPRIS)39236281},
      experiment   = {EXP:(DE-MLZ)NOSPEC-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {36044337},
      UT           = {WOS:000880288100008},
      doi          = {10.1091/mbc.E22-05-0152},
      url          = {https://bib-pubdb1.desy.de/record/604258},
}