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Manuel A. Friese (1973-)

Neurowissenschaftler

Name	Manuel A. Friese
Zeit	1973- (Lebensdaten)
Ort	Deutschland
Geschlecht	männlich
Akademischer Grad bzw. Titel	Dr.
Beruf	Neurowissenschaftler (charakteristischer Beruf)
Variante	M. A. Friese Manuel Alexander Friese Manuel Friese
Beziehung	Universitätsklinikum Hamburg-Eppendorf Universität Hamburg. Zentrum für Molekulare Neurobiologie
Weitere Angaben	Diss. Fachbereich Medizin, Hamburg, Univ., 2001 Univ. Hamburg, Medizinische Fak., Universitätsklinikum Hamburg-Eppendorf, Zentrum für Molekulare Neurobiologie, Leiter der Emmy Noether Research Group Neuroimmunology, 2008-
Quelle	http://www.zmnh.uni-hamburg.de/zmnh/groups/friese/friese_cv.html
Datensatztyp	Person
GND-Nummer	124101151
Datensatz-ID	124101151
Beteiligt an alle anzeigen Microglial complex I activity: a crucial factor for smoldering inflammation in the central nervous system The neuropathobiology of multiple sclerosis Sex- and species-specific contribution of CD99 to T cell costimulation during multiple sclerosis 14-3-3 $$\upzeta /\updelta$$ ζ Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease Author Correction: Pathogenetic mechanisms and treatment targets in cerebral malaria Vagus nerve inflammation contributes to dysautonomia in COVID-19 Jacob‐induced transcriptional inactivation of CREB promotes Aβ‐induced synapse loss in Alzheimer's disease Autologous haematopoietic stem cell transplantation for multiple sclerosis: a position paper and registry outline Autologous haematopoietic stem cell transplantation for multiple sclerosis: a position paper and registry outline Deciphering cAMP-dependent mechanisms for T cell regulation in the context of multiple sclerosis Stimulation and inhibition of protein-protein interactions to modulate autophagic pathways Neuronal metabotropic glutamate receptor 8 protects against neurodegeneration in CNS inflammation Quantitative study of the natural history of late-infantile neuronal ceroid lipofuscinosis (CLN2 disease) : a basis for evaluating experimental therapies The role of CLN3 in the lysosomal-autophagosomal system Control of SARS-CoV-2 infection in rituximab-treated neuroimmunological patients Funktionelle und strukturelle Konnektivität als Korrelate der kognitiven Leistung bei schubförmig remittierender Multipler Sklerose mit leichter Beeinträchtigung Genetic determinants of the humoral immune response in MS Sunlight exposure exerts immunomodulatory effects to reduce multiple sclerosis severity Untersuchung zur Assoziation vom HLA-DR15 Haplotyp und der Progression der Multiplen Sklerose Bassoon proteinopathy drives neurodegeneration in multiple sclerosis Arc/Arg3.1 defines dendritic cells and Langerhans cells with superior migratory ability independent of phenotype and ontogeny in mice Regulation of autoimmune neuroinflammation by Hv1 proton channels Translatome analysis of inflammatory neurodegeneration Untersuchungen zum Einfluss des Trpv4-Ionenkanals auf eine entzündungsgebundene Neurodegeneration des ZNS Sex differences in autoimmune disorders of the central nervous system Male offspring born to mildly ZIKV-infected mice are at risk of developing neurocognitive disorders in adulthood Regulation und Expression der Komplementproteine Faktor H und FHL-1-Reconectin in physiologischen und pathologischen Prozessen Regulation und Expression der Komplementproteine Faktor H und FHL-1-Reconectin in physiologischen und pathologischen Prozessen

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Katalog der Deutschen Nationalbibliothek

Manuel A. Friese (1973-)

Microglial complex I activity: a crucial factor for smoldering inflammation in the central nervous system

The neuropathobiology of multiple sclerosis

Sex- and species-specific contribution of CD99 to T cell costimulation during multiple sclerosis

14-3-3 $$\upzeta /\updelta$$ ζ

Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease

Author Correction: Pathogenetic mechanisms and treatment targets in cerebral malaria

Vagus nerve inflammation contributes to dysautonomia in COVID-19

Jacob‐induced transcriptional inactivation of CREB promotes Aβ‐induced synapse loss in Alzheimer's disease

Autologous haematopoietic stem cell transplantation for multiple sclerosis: a position paper and registry outline

Autologous haematopoietic stem cell transplantation for multiple sclerosis: a position paper and registry outline

Deciphering cAMP-dependent mechanisms for T cell regulation in the context of multiple sclerosis

Stimulation and inhibition of protein-protein interactions to modulate autophagic pathways

Neuronal metabotropic glutamate receptor 8 protects against neurodegeneration in CNS inflammation

Quantitative study of the natural history of late-infantile neuronal ceroid lipofuscinosis (CLN2 disease) : a basis for evaluating experimental therapies

The role of CLN3 in the lysosomal-autophagosomal system

Control of SARS-CoV-2 infection in rituximab-treated neuroimmunological patients

Funktionelle und strukturelle Konnektivität als Korrelate der kognitiven Leistung bei schubförmig remittierender Multipler Sklerose mit leichter Beeinträchtigung

Genetic determinants of the humoral immune response in MS

Sunlight exposure exerts immunomodulatory effects to reduce multiple sclerosis severity

Untersuchung zur Assoziation vom HLA-DR15 Haplotyp und der Progression der Multiplen Sklerose

Bassoon proteinopathy drives neurodegeneration in multiple sclerosis

Arc/Arg3.1 defines dendritic cells and Langerhans cells with superior migratory ability independent of phenotype and ontogeny in mice

Regulation of autoimmune neuroinflammation by Hv1 proton channels

Translatome analysis of inflammatory neurodegeneration

Untersuchungen zum Einfluss des Trpv4-Ionenkanals auf eine entzündungsgebundene Neurodegeneration des ZNS

Sex differences in autoimmune disorders of the central nervous system

Male offspring born to mildly ZIKV-infected mice are at risk of developing neurocognitive disorders in adulthood

Regulation und Expression der Komplementproteine Faktor H und FHL-1-Reconectin in physiologischen und pathologischen Prozessen

Regulation und Expression der Komplementproteine Faktor H und FHL-1-Reconectin in physiologischen und pathologischen Prozessen