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  • 1
    Electronic Resource
    Electronic Resource
    The twitcher mouse: An ultrastructural study on the oligodendroglia (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 159-166 
    Details
    ISSN: 1432-0533
    Keywords: Twitcher mouse ; Oligodendroglia ; Cellular degeneration ; Myelin sheaths ; Globoid cell leukodystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Morphological alterations of oligodendroglia were investigated in the spinal cord of the twitcher mouse, an authentic murine model of human globoid cell leukodystrophy (GLD) from day 5 to day 45 postnatal (p.n.). Typical inclusions were seen in the perikarya as well as the processes of oligodendroglia after day 10 with increasing frequency. The majority of the inclusions was non-crystalloid but rather needle-like or slender tubular in appearance. Ultrastructural features of cellular degeneration became first noticeable on days 25–30 in the oligodendroglial cytoplasm. These consisted of an increased number of microtubules and/or smooth cisterns, dispersed ribosomes, alteration of endoplasmic reticulum forming stacked lamellae or whorles, vesiculation or vacuolation of cytoplasm. The number of degenerating oligodendroglia increased in the older twitcher mice, so did the degenerating myelin sheath. However, even on day 45, when globoid cells became conspicuous in subpial and perivascular regions, many oligodendroglia and myelin sheaths were still well preserved. These observations suggested that oligodendrogial degeneration resulted in the degeneration of myelin sheaths but globoid cells appeared even before morphological evidence of myelin degeneration, presumably in response to the biochemical alterations resulted from the deficiency of galactosylceramidase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00703199
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  • 2
    Electronic Resource
    Electronic Resource
    Demyelination in the spinal cord of murine globoid cell leukodystrophy (the twitcher mouse) (1984)
    Springer
    Acta neuropathologica 62 (1984), S. 298-308 
    Details
    ISSN: 1432-0533
    Keywords: Globoid cell leukodystrophy ; Twitcher mouse ; Demyelination ; Spinal cord
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chronologic events of demyelination were investigated in the spinal cord of the twicher mouse, an authentic murine model of human globoid cell leukodystrophy (GLD) from 5 to 45 days postnatal. There was very little evidence of myelin degeneration before day 25 although clustered or scattered globoid cells were already noted in the dorsal columns and intramedullary portion of the ventral roots. Globoid cells contained typical cytoplasmic inclusions and in those which were found adjacent to degenerating myelin and naked axons, myelin debris were conspicuous in their cytoplasm. Vesiculation of myelin and a feature of globoid cells stripping myelin lamellae were noted in the area of demyelination. Myelin and oligodendroglial degeneration became pronounced throughout the spinal white matter after day 40 but globoid cells tended to be more concentrated in the dorsal columns. Our observations suggest that the emergence of globoid cells in GLD is in response to the changes in biochemical environment (i.e., excessive presence of galactosylceramide in the tissue?), and these cells appear to have a role as phagocytic cells in removing myelin lamellae.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687612
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  • 3
    Electronic Resource
    Electronic Resource
    Globoid cell leukodystrophy: Specialized contact of globoid cell with astrocyte in the brain of twitcher mouse (1982)
    Springer
    Acta neuropathologica 58 (1982), S. 237-242 
    Details
    ISSN: 1432-0533
    Keywords: Membrane specialization ; Globoid cell ; Astrocyte ; Globoid cell leukodystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Subplasmalemmal linear densities (Yajima et al. 1977 a) were the membrane specializations observed in globoid cells in globoid cell leukodystrophy (GLD) and in the cells of the mononuclear phagocytic system (Kawanami et al. 1980). In the spinal cord of the twitcher mouse, an authentic murine model of GLD, somewhat similar membrane specializations were noted in astrocytes, and on some occasions, a spot desmosome-like cellular contact was observed between globoid cells, which were likely to be mesodermal in origin, and astrocytes, which are of ectodermal origin. Possible significance of such apparent cellular contact is discussed briefly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688603
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  • 4
    Electronic Resource
    Electronic Resource
    Desensitization of the epidermal adenylate cyclase system: agonists and phorbol esters desensitize by independent mechanisms
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Molecular Cell Research 1093 (1991), S. 95-101 
    Details
    ISSN: 0167-4889
    Keywords: (Pig epidermis) ; Adenylate cyclase ; Agonist ; Desensitization ; Phorbol ester
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0167-4889(91)90143-L
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  • 5
    Electronic Resource
    Electronic Resource
    CRP down-regulates adenylate cyclase activity by reducing the level of phosphorylated IIAGlc, the glucose-specific phosphotransferase protein, in Escherichia coli (1998)
    Springer
    Molecular genetics and genomics 259 (1998), S. 317-326 
    Details
    ISSN: 1617-4623
    Keywords: Key words cAMP level ; Adenylate cyclase ; CRP ; Phosphorylation state ; IIAGlc
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The cellular cAMP level is markedly down-regulated by cAMP receptor protein (CRP) in Escherichia coli. CRP regulates adenylate cyclase both at the level of transcription of its structural gene cya and at the level of enzyme activity. We established a method to determine the phosphorylation state of IIAGlc, the glucose-specific phosphotransferase protein, in intact cells. We found that IIAGlc exists predominantly in the unphosphorylated form in wild-type cells growing in LB medium, while it is largely phosphorylated in crp or cya cells. Disruption of the ptsG gene that codes for the membrane component of the major glucose transporter (IICBGlc), and/or the fruF gene coding for FPr (fructose-specific hybrid phosphotransferase protein), did not affect the phosphorylation state of IIAGlc. When IICBGlc was overproduced in the presence of glucose, the levels of both cAMP and phosphorylated IIAGlc in crp cells were concomitantly decreased to wild-type levels. In addition, when His-90 in IIAGlc was replaced by glutamine, both phosphorylation of IIAGlc and the overproduction of cAMP in crp cells were eliminated. We also found that extracts of crp + cells markedly stimulate dephosphorylation of IIAGlc-P in vitro. We conclude that CRP-cAMP down-regulates adenylate cyclase primarily by reducing the level of phosphorylated IIAGlc. The data suggest that unspecified proteins whose expression is under the control of CRP-cAMP are responsible for this regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004380050818
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  • 6
    Electronic Resource
    Electronic Resource
    Protein kinase C-dependent modulation of stimulatory guanine nucleotide binding protein of fetal rat skin keratinocytes (1995)
    Springer
    Archives of dermatological research 288 (1995), S. 24-30 
    Details
    ISSN: 1432-069X
    Keywords: Key words G-protein ; Adenylate cyclase ; Phorbol ; esters ; Densensitization ; Keratinocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although the protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA) has been known to induce heterologous desensitization of the epidermal adenylate cyclase, the precise mechanism of PMA action remains unknown. Effects of PMA on the receptor-G-protein-adenylate cyclase system of fetal rat skin keratinocytes (FRSK) were investigated. Choleratoxin catalysed the ADP ribosylation of 45 kDa and 52 kDa membrane proteins and islet activating protein (IAP) catalysed the ADP ribosylation of a 40 kDa membrane protein. Incubation of FRSK with PMA decreased the cholera toxin-catalysed ADP ribosylation of the membrane protein, but not the IAP-catalysed ADP ribosylation. The effect of PMA on the cholera toxin-catalysed ADP ribosylation was inhibited by the PKC inhibitor, H-7 (1-(5-isoquinolinesulfonyl)-2-methyl piperazine dihydrochloride). 1-Oleoyl-2-acetylglycerol (OAG), a membrane-permeable diacylglycerol analogue, also decreased the cholera toxin-catalysed ADP ribosylation, but 4- O -methyl PMA, a very weak PKC activator, had no effect. Keratinocytes are known to express the guanine nucleotide binding proteins, Gsα, Gi2α and Gi3α. Immunoblot analysis of the PMA-treated FRSK showed no detectable difference in the amount of Gsα, Gi2α, Gi3α or the β subunit of the G-protein. PMA significantly decreased the β-adrenergic adenylate cyclase response and cholera toxin-induced cyclic AMP accumulation, while it markedly increased forskolin-induced cyclic AMP accumulation. These results indicate that phorbol esters affect the stimulatory guanine nucleotide binding protein (Gs) of FRSK via a PKC-dependent pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030050018
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