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Rickmann, Michael J.
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Rickmann, Michael J.
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Rickmann, Michael J.
Alternative Name
Rickmann, M. J.
Rickmann, Michael
Rickmann, M.
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2004Journal Article [["dc.bibliographiccitation.firstpage","229"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurogenetics"],["dc.bibliographiccitation.lastpage","238"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mannan, Ashraf U."],["dc.contributor.author","Roussa, Eleni"],["dc.contributor.author","Kraus, Cornelia"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Maenner, Joerg"],["dc.contributor.author","Nayernia, K."],["dc.contributor.author","Krieglstein, Kerstin"],["dc.contributor.author","Reis, A."],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T10:43:34Z"],["dc.date.available","2018-11-07T10:43:34Z"],["dc.date.issued","2004"],["dc.description.abstract","We report a novel spontaneous mutation named nax in mice, which exhibit delayed hair appearance and ataxia in a homozygote state. Histological analyses of nax brain revealed an overall impairment of the cerebellar cortex. The classical cortical cytoarchitecture was disrupted, the inner granule cell layer was not obvious, the Purkinje cells were not aligned as a Purkinje cell layer, and Bergmann glias did not span the molecular layer. Furthermore, histological analyses of skin showed that the hair follicles were also abnormal. We mapped the nax locus between marker D2Mit158 and D2Mit100 within a region of 800 kb in the middle of chromosome 2 and identified a missense mutation (Gly244Glu) in Acp2, a lysosomal monoesterase. The Glu244 mutation does not affect the stability of the Acp2 transcript, however it renders the enzyme inactive. Ultrastructural analysis of nax cerebellum showed lysosomal storage bodies in nucleated cells, suggesting progressive degeneration as the underlying mechanism. Identification of Acp2 as the gene mutated in nax mice provides a valuable model system for studying the role of Acp2 in cerebellum and skin homeostasis."],["dc.identifier.doi","10.1007/s10048-004-0197-9"],["dc.identifier.isi","000226285100005"],["dc.identifier.pmid","15503243"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47086"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1364-6745"],["dc.title","Mutation in the gene encoding lysosomal acid phosphatase (Acp2) causes cerebellum and skin malformation in mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2006Journal Article [["dc.bibliographiccitation.firstpage","253"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","262"],["dc.bibliographiccitation.volume","323"],["dc.contributor.author","Oehlke, O."],["dc.contributor.author","Sprysch, P."],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Roussa, Eleni"],["dc.date.accessioned","2018-11-07T10:21:05Z"],["dc.date.available","2018-11-07T10:21:05Z"],["dc.date.issued","2006"],["dc.description.abstract","Acute metabolic acidosis and alkalosis cause a series of homeostatic adaptive responses in the kidney and other epithelia. We hypothesized that acid/base disturbances might affect the expression of Na+/H+ stop exchanger (NHE) isoforms in salivary glands and determined the expression and cellular distribution of NHE3 and NHE4 in rat submandibular glands of controls and after imposed acute or chronic metabolic acidosis or alkalosis in vivo. Reverse transcription/polymerase chain reaction, in situ hybridization, and immunohistochemistry were applied by using specific primers, antisense probes, and antibodies, respectively. The results showed NHE3 and NHE4 transcript expression and protein abundance in rat submandibular gland. NHE3 was apically localized in duct cells, whereas NHE4 was found basolaterally distributed in acinar and duct cells. Acute acidosis and alkalosis and chronic acidosis had no effect on NHE3 and NHE4 expression and localization. In contrast, chronic metabolic alkalosis significantly decreased the number of apically stained NHE3 duct cells but had no effect on NHE3 mRNA expression. The results demonstrate, for the first time, the presence of NHE4 protein in salivary glands. The data also indicate the distinct regulation and adaptive changes of different isoforms of the same transporter in rat submandibular gland as a response to acid/base disturbances."],["dc.identifier.doi","10.1007/s00441-005-0055-6"],["dc.identifier.isi","000234689500007"],["dc.identifier.pmid","16158325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42024"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.title","Na+/H+ exchanger isoforms are differentially regulated in rat submandibular gland during acid/base disturbances in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2007Journal Article [["dc.bibliographiccitation.firstpage","1220"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","1231"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Rickmann, Michael"],["dc.contributor.author","Orlowski, B."],["dc.contributor.author","Heupel, Katharina"],["dc.contributor.author","Roussa, Eleni"],["dc.date.accessioned","2018-11-07T11:02:20Z"],["dc.date.available","2018-11-07T11:02:20Z"],["dc.date.issued","2007"],["dc.description.abstract","The electrogenic Na+/HCO3- cotransporter (NBCe1) has been identified as a key player for regulation of intracellular pH in several cell types. The present study was undertaken to determine expression and subcellular localization of the NH2- terminal solute carrier (SLC) 4A4 variants NBCe1-A and NBCe1-B in mouse brain using variant-specific antibodies by immunohistochemistry and immunoelectron microscopy. In addition, distribution of NBCe1 variants and activity-dependent regulation was investigated in mouse embryonic day 17.5 (E17.5) hippocampal primary cultures in vitro. The results showed NBCe1-A and NBCe1-B transcript expression in the mouse olfactory bulb, cerebral cortex, hippocampus and cerebellum. NBCe1-A was predominantly expressed in Purkinje cells, granule cells of the dentate gyrus, non-pyramidal cell bodies in cerebral cortex, and in periglomerular and mitral cells in the olfactory bulb. Pyramidal neurons in cerebral cortex and apical cell dendrites in the hippocampus were stained for both NBCe1-A and NBCe1-B. Moreover, NBCe1-B was present in Bergmann glia. At the ultrastructural level, NBCe1-B was preferentially expressed in perivascular astroglial lamellae, whereas both NBCe1 NH2-terminal variants were localized in pre- and postsynaptic compartments. Except for the olfactory bulb, NBCe1-A was always colocalized with calbindin. Treatment of E17.5 primary hippocampal cultures with KCl, showed dramatic downregulation of NBCe1-B mRNA and protein after 60 min, whereas NBCe1-A expression remained unchanged. These data demonstrate for the first time distinct cellular distribution of NBCe1 NH2-terminal variants in mouse brain. NBCe1 may be involved in neuronal modulation, and pH regulation during neuronal activity. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuroscience.2007.02.061"],["dc.identifier.isi","000246584500030"],["dc.identifier.pmid","17433553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51358"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0306-4522"],["dc.title","Distinct expression and subcellular localization patterns of NA(+)/HCO3- cotransporter (SLC 4A4) variants NBCe1-A and NBCe1-B in mouse brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS