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  • 1
    Electronic Resource
    Electronic Resource
    Neurotrophins prevent HIV Tat-induced neuronal apoptosis via a nuclear factor-κB (NF-κB)-dependent mechanism (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: HIV-1 associated dementia is thought to be caused by neuronal damage and death in response to the production of soluble neurotoxic factors by virally infected mononuclear phagocytes. These neurotoxins include HIV-1 Tat. The ability of neurotrophins to promote cell survival prompted us to examine whether neurotrophins might also be capable of opposing the pro-apoptotic effects of Tat. Here, we show that Tat-induced neuronal apoptosis in primary cultures of rat cerebellar granule cells and in neuronally differentiated human SK-N-MC cells is profoundly inhibited by brain-derived neurotrophic factor, nerve growth factor and activity-dependent neurotrophic factor nonamer peptide. These neurotrophins activated the transcription factor NF-κB, and inhibition of NF-κB activation using a super-repressor IκB-α mutant was found to block the survival-promoting activity of the neurotrophins. Reporter gene assays and immunoblot experiments revealed that the neurotrophins also up-regulated the expression of Bcl-2, at both the transcriptional and protein levels. Overexpression of the super-repressor IκB-α mutant prevented this induction of Bcl-2 expression. Moreover, overexpression of either Bcl-2, alone, or the RelA subunit of NF-κB, alone, protected neurons from Tat-induced apoptosis. These findings suggest that the activation of NF-κB by neurotrophic factors may promote survival of neurons exposed to Tat, via regulation of anti-apoptotic genes including Bcl-2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00467.x
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    HIV-1 Tat-Mediated Activation of Glycogen Synthase Kinase-3β Contributes to Tat-Mediated Neurotoxicity (1999)
    Oxford UK : Blackwell Science Ltd.
    Journal of neurochemistry 73 (1999), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : Human immunodeficiency virus type 1 (HIV-1) Tat induces neuronal apoptosis. To examine the mechanism(s) that contribute to this process, we studied Tat's effects on glycogen synthase kinase-3β (GSK-3β), an enzyme that has been implicated in the regulation of apoptosis. Addition of Tat to rat cerebellar granule neurons resulted in an increase in GSK-3β activity, which was not associated with a change in protein expression and could be abolished by the addition of an inhibitor of GSK-3β (lithium). Lithium also enhanced neuronal survival following exposure to Tat. Coprecipitation experiments revealed that Tat can associate with GSK-3β, but direct addition of Tat to purified GSK-3β had no effect on enzyme activity, suggesting that Tat's effects might be mediated indirectly. As the activation of platelet activating factor (PAF) receptors is critical for the induction of neuronal death by several candidate HIV-1 neurotoxins, we determined whether PAF can also activate GSK-3β. Application of PAF to neuronal cultures activated GSK-3β, and coincubation with lithium ameliorated PAF-induced neuronal apoptosis. These findings are consistent with the existence of one or more pathways that can lead to GSK-3β activation in neurons, and they suggest that the dysregulation of this enzyme could contribute to HIV-induced neuronal apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1999.0730578.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Functional Interplay Between Nuclear Factor-κB and c-Jun Integrated by Coactivator p300 Determines the Survival of Nerve Growth Factor-Dependent PC12 Cells (2000)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 74 (2000), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Nerve growth factor (NGF) activates the transcription factors nuclear factor κB (NF-κB) and activator protein-1 (AP-1) in sympathetic neurons. Whereas NGF-inducible NF-κB is required for the survival of neurons, c-Jun has the ability to promote neuronal death. In this report, we have examined the effect of NGF withdrawal on c-Jun and NF-κB transcription factors in PC12 cells differentiated to a neuronal phenotype. We show that the withdrawal of NGF from these cultures results in de novo synthesis of c-Jun, increase in AP-1 activity, and down-regulation of NF-κB activity. To investigate how the signal transduction pathways activating c-Jun and NF-κB are differentially regulated by NGF, we performed transcriptional analyses. Expression of RelA (NF-κB) suppressed the c-Jun-dependent transcription of c-jun, and this effect was reversed by overexpression of the coactivator p300. RelA’s effects on c-Jun transcription were mediated by competitive binding of the carboxy-terminal region of RelA to the CH1 domain of p300, which also binds to c-Jun; deletion of this region abrogated the ability of RelA to inhibit c-Jun activity. Furthermore, the inhibition of endogenous NF-κB in NGF-maintained neuronal PC12 cells led to the induction of c-Jun synthesis and a marked increase in cell death. Together, these studies demonstrate a functional interaction between NF-κB and c-Jun and suggest a novel mechanism of NF-κB-mediated neuroprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2000.740527.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Activation of glycogen synthase kinase 3 beta (GSK-3β) by platelet activating factor mediates migration and cell death in cerebellar granule neurons (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Children with vertically acquired HIV-1 can present with a rapidly progressive encephalopathy and neuronal apoptosis in the first 12–18 months of life. Furthermore, abnormal prenatal platelet activating factor (PAF) signalling may result in lissencephaly, a disorder of neuronal migration. PAF, produced from human immunodeficiency virus type 1 (HIV-1) -infected brain-resident macrophages, induces neuronal apoptosis in cultured cerebellar granule neurons (CGNs) in part by activating glycogen synthase kinase 3 beta (GSK-3β). However, PAF can also inhibit migration of CGNs that are dispersed and allowed to reaggregate. Therefore, we investigated the biological effects following activation of GSK-3β by PAF, and whether these effects were dependent on the culture conditions of the CGNs. We show here that activation of neuronal GSK-3β by PAF is receptor-specific, with similar kinetics of activation in both monolayer cultures of CGNs that have ceased to migrate and reaggregate cultures of CGNs that are actively migrating. However, PAF receptor activation in reaggregated CGNs inhibits neuronal migration and induces approximately half the level of neuronal apoptosis compared with PAF-treated CGN cultures that have ceased to migrate. PAF-mediated inhibition of neuronal migration in reaggregated CGNs or induction of apoptosis in CGNs that have ceased to migrate can be reversed by either PAF receptor antagonists, or the GSK-3β inhibitors lithium or valproic acid, in a dose-dependent manner. Abnormal PAF signalling that results in GSK-3β overactivation may represent a common mechanism for pathological defects in neuronal migration in the prenatal period and neuronal apoptosis in the postnatal period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0953-816x.2001.01572.x
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Sequence analysis and acute pathogenicity of molecularly cloned SIV SMM-PBj14 (1990)
    [s.l.] : Nature Publishing Group
    Nature 345 (1990), S. 636-640 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/345636a0
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    Paper (German National Licenses)
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  • 6
    Book
    Book
    C++ gotchas : Avoiding common problems in coding and design (2003)
    Boston [u.a.] :Addison-Wesley,
    Details
    Title: C++ gotchas : Avoiding common problems in coding and design
    Author: Dewhurst, Stephen C.
    Publisher: Boston [u.a.] :Addison-Wesley,
    Year of publication: 2003
    Pages: XVI, 325 S.
    Series Statement: Addison-Wesley professional computing series
    ISBN: 0-321-12518-5
    Type of Medium: Book
    Language: English
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