@Article{macau_mods_00003034,
  author = 	{Adamski, Vivian
		and Mentlein, Rolf
		and Lucius, Ralph-Erich
		and Synowitz, Michael
		and Held-Feindt, Janka
		and Hattermann-Koch, Kirsten},
  title = 	{The Chemokine Receptor CXCR6 Evokes Reverse Signaling via the Transmembrane Chemokine CXCL16},
  journal = 	{International journal of molecular sciences},
  year = 	{2017},
  publisher = 	{MDPI AG},
  address = 	{Basel},
  volume = 	{18},
  number = 	{7},
  keywords = 	{Humans; Glioma; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Receptors, Chemokine; Cell Communication; Signal Transduction; Cell Movement; Phosphorylation; Chemokine CXCL16; Receptors, CXCR6},
  abstract = 	{Reverse signaling is a signaling mechanism where transmembrane or membrane-bound ligands transduce signals and exert biological effects upon binding of their specific receptors, enabling a bidirectional signaling between ligand and receptor-expressing cells. In this study, we address the question of whether the transmembrane chemokine (C-X-C motif) ligand 16, CXCL16 is able to transduce reverse signaling and investigate the biological consequences. For this, we used human glioblastoma cell lines and a melanoma cell line as in vitro models to show that stimulation with recombinant C-X-C chemokine receptor 6 (CXCR6) or CXCR6-containing membrane preparations induces intracellular (reverse) signaling. Specificity was verified by RNAi experiments and by transfection with expression vectors for the intact CXCL16 and an intracellularly-truncated form of CXCL16. We showed that reverse signaling via CXCL16 promotes migration in CXCL16-expressing melanoma and glioblastoma cells, but does not affect proliferation or protection from chemically-induced apoptosis. Additionally, fast migrating cells isolated from freshly surgically-resected gliomas show a differential expression pattern for CXCL16 in comparison to slowly-migrating cells, enabling a possible functional role of the reverse signaling of the CXCL16/CXCR6 pair in human brain tumor progression in vivo.},
  issn = 	{1661-6596},
  doi = 	{10.3390/ijms18071468},
  url = 	{https://macau.uni-kiel.de/receive/macau_mods_00003034},
  url = 	{https://doi.org/10.3390/ijms18071468},
  url = 	{http://www.ncbi.nlm.nih.gov/pubmed/28698473},
  file = 	{:https://macau.uni-kiel.de/servlets/MCRFileNodeServlet/macau_derivate_00004181/ijms-18-01468.pdf:PDF},
  language = 	{en}
}