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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2012-04-14
    Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Redmond, Stephanie A -- Chan, Jonah R -- R01 NS062796/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Apr 13;336(6078):161-2. doi: 10.1126/science.1221689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22499927" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging ; Animals ; Demyelinating Diseases/*physiopathology/therapy ; Macrophages/*physiology ; Mice ; Myelin Sheath/*physiology ; Oligodendroglia/*physiology ; Parabiosis ; Phagocytosis ; Spinal Cord Diseases/*physiopathology/therapy
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 2002-11-09
    Beschreibung: Schwann cells in developing and regenerating peripheral nerves express elevated levels of the neurotrophin receptor p75NTR. Neurotrophins are key mediators of peripheral nervous system myelination. Our results show that myelin formation is inhibited in the absence of functional p75NTR and enhanced by blocking TrkC activity. Moreover, the enhancement of myelin formation by endogenous brain-derived neurotrophic factor is mediated by the p75NTR receptor, whereas TrkC receptors are responsible for neurotrophin-3 inhibition. Thus p75NTR and TrkC receptors have opposite effects on myelination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cosgaya, Jose M -- Chan, Jonah R -- Shooter, Eric M -- NS04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2002 Nov 8;298(5596):1245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Fairchild Building, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12424382" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Antibodies/immunology ; Axons/physiology ; Brain-Derived Neurotrophic Factor/pharmacology/physiology ; Coculture Techniques ; Ganglia, Spinal/cytology ; Immunohistochemistry ; Mice ; Models, Neurological ; Myelin P0 Protein/metabolism ; Myelin Sheath/*physiology ; Myelin-Associated Glycoprotein/metabolism ; Neurotrophin 3/pharmacology/physiology ; Rats ; Rats, Sprague-Dawley ; Receptor, Nerve Growth Factor ; Receptor, trkB/metabolism ; Receptor, trkC/metabolism ; Receptors, Nerve Growth Factor/immunology/*physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Schwann Cells/*physiology ; Sciatic Nerve/cytology/metabolism ; Signal Transduction
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
    Publikationsdatum: 2006-11-04
    Beschreibung: Cell polarity is critical in various cellular processes ranging from cell migration to asymmetric cell division and axon and dendrite specification. Similarly, myelination by Schwann cells is polarized, but the mechanisms involved remain unclear. Here, we show that the polarity protein Par-3 localizes asymmetrically in Schwann cells at the axon-glial junction and that disruption of Par-3 localization, by overexpression and knockdown, inhibits myelination. Additionally, we show that Par-3 directly associates and recruits the p75 neurotrophin receptor to the axon-glial junction, forming a complex necessary for myelination. Together, these results point to a critical role in the establishment of cell polarity for myelination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chan, Jonah R -- Jolicoeur, Christine -- Yamauchi, Junji -- Elliott, Jimmy -- Fawcett, James P -- Ng, Benjamin K -- Cayouette, Michel -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):832-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Neurobiology, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles 90089, USA. jonah.chan@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082460" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Amino Acid Motifs ; Animals ; Axons/chemistry/ultrastructure ; Brain-Derived Neurotrophic Factor/physiology ; Carrier Proteins/analysis/chemistry/genetics/*metabolism ; *Cell Polarity ; Cells, Cultured ; Coculture Techniques ; Ganglia, Spinal/ultrastructure ; Intercellular Junctions/chemistry ; Mice ; Myelin Sheath/*physiology ; Nerve Tissue Proteins/chemistry/*metabolism ; Protein Structure, Tertiary ; Rats ; Receptors, Growth Factor/chemistry/*metabolism ; Schwann Cells/cytology/*physiology/ultrastructure
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
    Publikationsdatum: 2016-01-23
    Beschreibung: Oligodendrocytes myelinate axons in the central nervous system and develop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain and spinal cord development. We show that OPCs require the vasculature as a physical substrate for migration. We observed that OPCs of the embryonic mouse brain and spinal cord, as well as the human cortex, emerge from progenitor domains and associate with the abluminal endothelial surface of nearby blood vessels. Migrating OPCs crawl along and jump between vessels. OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes. Thus, physical interactions with the vascular endothelium are required for OPC migration. We identify Wnt-Cxcr4 (chemokine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signaling coordinates OPC migration with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Niu, Jianqin -- Munji, Roeben -- Davalos, Dimitrios -- Chang, Junlei -- Zhang, Haijing -- Tien, An-Chi -- Kuo, Calvin J -- Chan, Jonah R -- Daneman, Richard -- Fancy, Stephen P J -- 1P01 NS083513/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):379-84. doi: 10.1126/science.aad3839.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. ; Departments of Pharmacology and Neuroscience, University of California at San Diego (UCSD), San Diego, CA 92093, USA. ; Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. Department of Urology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Howard Hughes Medical Institute (HHMI), Chevy Chase, MD 20815, USA. Duke University School of Medicine, Durham, NC 27710, USA. ; Department of Neurology, UCSF, San Francisco, CA 94158, USA. ; Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. Department of Neurology, UCSF, San Francisco, CA 94158, USA. Division of Neonatology, UCSF, San Francisco, CA 94158, USA. Newborn Brain Research Institute, UCSF, San Francisco, CA 94158, USA. stephen.fancy@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798014" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Blood Vessels/cytology/embryology ; *Cell Movement ; Cerebral Cortex/blood supply/*embryology ; Endothelium, Vascular/cytology ; Humans ; Mice ; Neural Stem Cells/cytology/*physiology ; *Neurogenesis ; Oligodendroglia/cytology/*physiology ; *Organogenesis ; Pericytes/cytology/physiology ; Receptors, CXCR4/metabolism ; Signal Transduction ; Spinal Cord/blood supply/cytology/*embryology ; Wnt Proteins/metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
    Publikationsdatum: 2018-04-13
    Beschreibung: Antibodies have the specificity to differentiate foreign antigens that mimic self antigens, but it remains unclear how such specificity is acquired. In a mouse model, we generated B cells displaying an antibody that cross-reacts with two related protein antigens expressed on self versus foreign cells. B cell anergy was imposed by self antigen but reversed upon challenge with high-density foreign antigen, leading to germinal center recruitment and antibody gene hypermutation. Single-cell analysis detected rapid selection for mutations that decrease self affinity and slower selection for epistatic mutations that specifically increase foreign affinity. Crystal structures revealed that these mutations exploited subtle topological differences to achieve 5000-fold preferential binding to foreign over self epitopes. Resolution of antigenic mimicry drove the optimal affinity maturation trajectory, highlighting the value of retaining self-reactive clones as substrates for protective antibody responses.
    Schlagwort(e): Cell Biology, Immunology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Geologie und Paläontologie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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