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  • 1995-1999  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Cytochrome c release and caspase-3 activation during colchicine-induced apoptosis of cerebellar granule cells (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The microtubule-disrupting agent colchicine is known to be neurotoxic toward certain neuronal populations including cerebellar granule cells (CGCs). In this study we investigated the involvement of cytochrome c release and caspase-3 activation during colchicine-induced CGC apoptosis. Treatment of rat CGCs with 1 μm colchicine (for up to 24 h) caused high molecular weight DNA fragmentation and nuclear condensation. An involvement of group II caspases (which includes caspase-3) was demonstrated by the proteolytic degradation of poly(ADP-ribose) polymerase (PARP) after 18 h exposure to colchicine. Colchicine induced a time-dependent increase in Ac-Asp-Glu-Val-Asp-α-(4-methyl-coumaryl-7-amide) (DEVD-MCA) cleavage activity in CGCs, which was blocked with a specific, peptide-based, aldehyde inhibitor of group II caspases, i.e. DEVD-CHO. We also observed a time-dependent proteolysis of caspase-3 as judged by the appearance of p17 which is one of the subunits of active caspase-3. Activation of caspase-3 during colchicine-induced apoptosis may be mediated by cytochrome c since there was a close correlation between the time courses of cytochrome c release from the mitochondria and of caspase-3 activation. Furthermore, colchicine-induced apoptosis, as assessed by propidium iodide visualization of the nuclei, could be blocked by the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp (O-methyl) fluoromethyl ketone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00512.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Neuronal apoptosis versus necrosis induced by glutamate or free radicals (1996)
    Springer
    Apoptosis 1 (1996), S. 5-10 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; excitotoxicity ; glutamate ; cytoskeleton ; nitric oxide ; NMDA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The type of cell death encountered in neuronal cell cultures exposed to excitatory amino acids — such as glutamate, the major excitatory neurotransmitter in the central nervous system, or free radicals, such as nitric oxide (NO.) and superoxide anoin (O2. −), which react to form peroxynitrite (ONOO−) — appears to depend on the intensity of the exposure and may involve two temporarily distinct phases. Following relatively fulminant insults, an initial phase of necrosis — associated with extreme energy depletion — may simply reflect the failure of neurons to carry out the ‘default’ apoptotic death program used to efficiently dispose of aged or otherwise unwanted cells. Neurons recovering mitochondrial energy potential after an initial fulminant insult or following a more subtle inciting injury may subsequently undergo apoptosis, possibly associated with a factor released from mitochondria that triggers this death program. The maintenance of balanced energy production may be a decisive factor in detemining the degree, type, and progression of neuronal injury caused by ‘excitotoxins’ and free radicals. Similar events could possibly occur in vivo after ischemia or other insults.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00142073
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Proteases in apoptosis (1996)
    Springer
    Cellular and molecular life sciences 52 (1996), S. 968-978 
    Details
    ISSN: 1420-9071
    Keywords: Apoptosis ; proteases ; ICE-like proteases ; protein substrates
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The interleukin-1 β-converting enzyme (ICE)-like family proteases have recently been identified as key enzymes in apoptotic cell death. Among these proteases one can identify specific activities which may be involved in cytokine production or in resident protein cleavage. Several factors influence the constitutive apoptotic mechanism and may provide insight into the role of protease(s) in apoptosis. Although it appears that ICE family members play a most important role in promoting apoptotic cell death, evidence has been advanced that other proteases are also involved in sequential or parallel steps of apoptosis. Activation of a particular protease can lead to processing molecules either of the same or different proteases, leading to an activation of a protease cascade. Here we attempt to summarize the current thinking concerning these proteases and their involvement in apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01920106
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    Paper (German National Licenses)
    Fulltext
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