@article{VamanVSPoppeHoubenetal.2015,
  author    = {Vaman V. S., Anjana and Poppe, Heiko and Houben, Roland and Grunewald, Thomas G. P. and Goebeler, Matthias and Butt, Elke},
  title     = {LASP1, a Newly Identified Melanocytic Protein with a Possible Role in Melanin Release, but Not in Melanoma Progression},
  series = {PLoS One},
  volume    = {10},
  journal   = {PLoS One},
  number    = {6},
  doi       = {10.1371/journal.pone.0129219},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125994},
  pages     = {e0129219},
  year      = {2015},
  abstract  = {The LIM and SH3 protein 1 (LASP1) is a focal adhesion protein. Its expression is increased in many malignant tumors. However, little is known about the physiological role of the protein. In the present study, we investigated the expression and function of LASP1 in normal skin, melanocytic nevi and malignant melanoma. In normal skin, a distinct LASP1 expression is visible only in the basal epidermal layer while in nevi LASP1 protein is detected in all melanocytes. Melanoma exhibit no increase in LASP1 mRNA compared to normal skin. In melanocytes, the protein is bound to dynamin and mainly localized at late melanosomes along the edges and at the tips of the cell. Knockdown of LASP1 results in increased melanin concentration in the cells. Collectively, we identified LASP1 as a hitherto unknown protein in melanocytes and as novel partner of dynamin in the physiological process of membrane constriction and melanosome vesicle release.},
  language  = {en}
}
@article{BuschWesthofenKochetal.2014,
  author    = {Busch, Martin and Westhofen, Thilo C. and Koch, Miriam and Lutz, Manfred B. and Zernecke, Alma},
  title     = {Dendritic Cell Subset Distributions in the Aorta in Healthy and Atherosclerotic Mice},
  series = {PLoS ONE},
  volume    = {9},
  journal   = {PLoS ONE},
  number    = {2},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0088452},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-119907},
  pages     = {e88452},
  year      = {2014},
  abstract  = {Dendritic cells (DCs) can be sub-divided into various subsets that play specialized roles in priming of adaptive immune responses. Atherosclerosis is regarded as a chronic inflammatory disease of the vessel wall and DCs can be found in non-inflamed and diseased arteries. We here performed a systematic analyses of DCs subsets during atherogenesis. Our data indicate that distinct DC subsets can be localized in the vessel wall. In C57BL/6 and low density lipoprotein receptor-deficient (Ldlr-/-) mice, CD11c+ MHCII+ DCs could be discriminated into CD103- CD11b+F4/80+, CD11b+F4/80- and CD11b-F4/80- DCs and CD103+ CD11b-F4/80- DCs. Except for CD103- CD11b- F4/80- DCs, these subsets expanded in high fat diet-fed Ldlr-/- mice. Signal-regulatory protein (Sirp)-α was detected on aortic macrophages, CD11b+ DCs, and partially on CD103- CD11b- F4/80- but not on CD103+ DCs. Notably, in FMS-like tyrosine kinase 3-ligand-deficient (Flt3l-/-) mice, a specific loss of CD103+ DCs but also CD103- CD11b+ F4/80- DCs was evidenced. Aortic CD103+ and CD11b+ F4/80- CD103- DCs may thus belong to conventional rather than monocyte-derived DCs, given their dependence on Flt3L-signalling. CD64, postulated to distinguish macrophages from DCs, could not be detected on DC subsets under physiological conditions, but appeared in a fraction of CD103- CD11b+ F4/80- and CD11b+ F4/80+ cells in atherosclerotic Ldlr-/- mice. The emergence of CD64 expression in atherosclerosis may indicate that CD11b+ F4/80- DCs similar to CD11b+ F4/80+ DCs are at least in part derived from immigrated monocytes during atherosclerotic lesion formation. Our data advance our knowledge about the presence of distinct DC subsets and their accumulation characteristics in atherosclerosis, and may help to assist in future studies aiming at specific DC-based therapeutic strategies for the treatment of chronic vascular inflammation.},
  language  = {en}
}