Research Topics
Genomes and Genes | Marco PrinzSummaryAffiliation: University Hospital Country: Germany Publications
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Publications
Tickets to the brain: role of CCR2 and CX3CR1 in myeloid cell entry in the CNSMarco Prinz
Department of Neuropathology, University of Freiburg, Breisacher Str 64, D 79106 Freiburg, Germany
J Neuroimmunol 224:80-4. 2010..Therefore, these molecules present viable targets for therapeutic manipulations of myeloid cells destined for the CNS...- Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous systemMarco Prinz
Department of Neuropathology, University of Freiburg, D 79106 Freiburg, Germany
Immunity 28:675-86. 2008..In contrast, absence of IFNAR on myeloid cells led to severe disease with an enhanced effector phase and increased lethality, indicating a distinct protective function of type I IFNs during autoimmune inflammation of the CNS... - Heterogeneity of CNS myeloid cells and their roles in neurodegenerationMarco Prinz
Department of Neuropathology, University Hospital of Freiburg, Freiburg, Germany
Nat Neurosci 14:1227-35. 2011..On the basis of these new studies, we differentiate brain myeloid subtypes with regard to their origin, function and fate in the brain and illustrate the divergent features of these cells during neurodegeneration... 
Comparative transcriptome profiling of amyloid precursor protein family members in the adult cortexDorothee Aydin
Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology, Heidelberg University, Im Neuenheimer Feld 364, D 69120 Heidelberg, Germany
BMC Genomics 12:160. 2011..The γ-secretase-generated APP intracellular domain (AICD) functions as a transcriptional regulator in heterologous reporter assays although its role for endogenous gene regulation has remained controversial...- Microglia in the CNS: immigrants from another worldMarco Prinz
Department of Neuropathology, University of Freiburg, Freiburg, Germany
Glia 59:177-87. 2011..These new aspects will be discussed in the present review... - New lessons about old molecules: how type I interferons shape Th1/Th17-mediated autoimmunity in the CNSMarco Prinz
Department of Neuropathology, University of Freiburg, Breisacher Str 64, D 79106 Freiburg, Germany
Trends Mol Med 16:379-86. 2010..The recent discovery of a novel T-cell subset, Th17 cells, sheds new light on type I IFNs in MS... - CCR2+Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous systemAlexander Mildner
Department of Neuropathology, University of Freiburg, Freiburg, Germany
Brain 132:2487-500. 2009..Collectively, these data indicate a disease-promoting role of CCR2+Ly-6Chi monocytes during autoimmune inflammation of the central nervous system... - Resistance to hypoxia-induced, BNIP3-mediated cell death contributes to an increase in a CD133-positive cell population in human glioblastomas in vitroUlf Dietrich Kahlert
Division of Stereotactic Neurosurgery, University Freiburg Medical Center, Freiburg, Germany
J Neuropathol Exp Neurol 71:1086-99. 2012..These results suggest the possible efficacy of a novel therapy for glioblastoma focused on eradication of BTSCs by modifications of epigenetic regulation of gene expression... - Cytosolic RIG-I-like helicases act as negative regulators of sterile inflammation in the CNSAngela Dann
Department of Neuropathology, University of Freiburg, Freiburg, Germany
Nat Neurosci 15:98-106. 2012.... - Distinct and non-redundant roles of microglia and myeloid subsets in mouse models of Alzheimer's diseaseAlexander Mildner
Department of Neuropathology, University of Freiburg, D 79106 Freiburg, Germany
J Neurosci 31:11159-71. 2011..Together, our data advocate selective functions of CCR2-expressing myeloid subsets, which could be targeted specifically to modify disease burden in AD... 
Ly-6G+CCR2- myeloid cells rather than Ly-6ChighCCR2+ monocytes are required for the control of bacterial infection in the central nervous systemAlexander Mildner
Department of Neuropathology, University of Freiburg, Freiburg, Germany
J Immunol 181:2713-22. 2008....- IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous systemJenni Raasch
Department of Neuropathology, University of Freiburg, Breisacher Str 64, D 79106 Freiburg, Germany
Brain 134:1184-98. 2011..Thus, therapies targeting IκB kinase 2 function in non-neuronal cells may represent a promising strategy for the treatment of distinct demyelinating central nervous system diseases... - Multi-focal occurrence of cortical dysplasia in epilepsy patientsSusanne Fauser
Epilepsy Center, Department of Neurosurgery, University of Freiburg, Breisacher Strasse 64, 79106 Freiburg, Germany
Brain 132:2079-90. 2009..Based on genetic analysis and clinical features, multi-FCD in this patient series was not likely to be related to tuberous sclerosis... - Microglia emerge from erythromyeloid precursors via Pu.1- and Irf8-dependent pathwaysKatrin Kierdorf
Department of Neuropathology, University of Freiburg, Freiburg, Germany
Nat Neurosci 16:273-80. 2013..Our data provide cellular and molecular insights into the origin and development of microglia... - How type I interferons shape myeloid cell function in CNS autoimmunityStefanie M Brendecke
Department of Neuropathology, University of Freiburg, Freiburg, Germany
J Leukoc Biol 92:479-88. 2012..This kind of approach would allow for replacing the current treatment strategy in MS of broadly and unselectively altering all immune responses, regardless of their beneficial or detrimental nature... - Activation of canonical WNT/β-catenin signaling enhances in vitro motility of glioblastoma cells by activation of ZEB1 and other activators of epithelial-to-mesenchymal transitionUlf D Kahlert
Division of Stereotactic Neurosurgery, Department of General Neurosurgery, University Medical Center Freiburg, Freiburg, Germany
Cancer Lett 325:42-53. 2012..These findings suggest that canonical WNT/β-catenin pathway is a critical regulator of GBM invasion and may represent a potential therapeutic target... - IκB-ζ deficiency leaves epithelial cells high and dryStefanie M Brendecke
Institute of Neuropathology, University of Freiburg, 79100 Freiburg, Germany
Immunity 38:404-6. 2013..2013) demonstrate that tissue-specific dysfunction, namely deficiency of the transcriptional regulator IκB-ζ in epithelial cells, rather than hematopoietic cell pathology, is sufficient to elicit SS-like inflammation... - Bone marrow cell recruitment to the brain in the absence of irradiation or parabiosis biasKatrin Kierdorf
Institute of Neuropathology, University of Freiburg, Freiburg, Germany Faculty of Biology, University of Freiburg, Freiburg, Germany
PLoS ONE 8:e58544. 2013.... - Type I interferons as ambiguous modulators of chronic inflammation in the central nervous systemMarco Prinz
Department of Neuropathology, University Clinic Freiburg Freiburg, Germany
Front Immunol 3:67. 2012..Recently uncovered molecular and cellular mechanisms in the etiology of AGS and experimental autoimmune encephalomyelitis (EAE), the murine model of MS will be highlighted... - mHERC6 is the essential ISG15 E3 ligase in the murine systemLars Ketscher
University Clinic Freiburg, Department of Neuropathology, Freiburg im Breisgau, Germany
Biochem Biophys Res Commun 417:135-40. 2012..We demonstrate that mHERC6 is essential for endogenous murine ISGylation and thus represents the dominant ISG15 E3 ligase in mice. In contrast to its human homologue, mHERC6 is also capable to mediate conjugation of human ISG15...