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  • Cerebral blood flow  (2)
  • DEATH
  • COMPLEXES
  • COMPLEX
Publisher
Years
  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CELL ; Germany ; INHIBITION ; PATHWAY ; DEATH ; PROTEIN ; RNA ; transcription ; ACTIVATION ; COMPLEX ; COMPLEXES ; FAMILY ; nuclear bodies ; COMPONENT ; MAMMALIAN-CELLS ; MITOCHONDRIA ; TRANSLOCATION ; GLUCOCORTICOID-RECEPTOR ; FLICE ; PML ; CD95 ; RE ; FAMILIES ; INTERFERENCE ; RNA INTERFERENCE ; CASPASE-8 ; MEDIATED APOPTOSIS ; senescence ; death receptor ; SIGNALS ; FLASH ; CD95 (Fas/APO-1)
    Abstract: Caspase-8-binding protein FLICE-associated huge protein ( FLASH) has been proposed to regulate death receptor CD95-induced apoptosis through facilitating caspase-8 activation at the death-inducing signaling complex. Here, we found that FLASH interacts with the PML nuclear body component Sp100 and predominantly resides in the nucleus and nuclear bodies (NBs). In response to CD95 activation, FLASH leaves the NBs and translocates into the cytoplasm where it accumulates at mitochondria. The nucleo-cytoplasmic translocation of FLASH requires CD95-induced caspase activation and is facilitated by the Crm1-dependent nuclear export pathway. Downregulation of FLASH by RNA interference or inhibition of its nucleocytoplasmic shuttling reduced CD95-induced apoptosis. Furthermore, we show that the adenoviral anti-apoptotic Bcl-2 family member E1B19K traps FLASH and procaspase-8 in a ternary complex at mitochondria, thereby blocking CD95-induced caspase-8 activation. Knock-down of Sp100 potentiated CD95-activated apoptosis through enhancing nucleo-cytoplasmic FLASH translocation. In summary, our findings suggest that CD95 signals via a previously unrecognized nuclear pathway mediated by nucleo-cytoplasmic translocation of FLASH
    Type of Publication: Journal article published
    PubMed ID: 17245429
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  • 2
    ISSN: 1432-1076
    Keywords: Phenobarbital ; Cerebral blood flow ; Newborn infants ; Foetal distress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of phenobarbital on cerebral blood flow (CBF) was investigated by the intravenous Xenon133 clearance technique in seven term newborn infants with signs of mild to moderate hypoxic ischaemic encephalopathy, all on sustained spontaneous ventilation. Phenobarbital treatment had no significant effect on CBF 60 min after loading dosage (20mg/kg i.v.). Likewise, no significant change in mean arterial blood pressure, heart rate or transcutaneous gas tensions was observed. Though slight changes in CBF of short duration cannot be excluded, conventional dosage of phenobarbital to term newborn infants with foetal distress apparently imposes no risk of cerebrovascular damage.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1076
    Keywords: Key words     Phenobarbital ; Cerebral blood flow ; Newborn infants ; Foetal distress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract      The effect of phenobarbital on cerebral blood flow (CBF) was investigated by the intravenous Xenon133 clearance technique in seven term newborn infants with signs of mild to moderate hypoxic ischaemic encephalopathy, all on sustained spontaneous ventilation. Phenobarbital treatment had no significant effect on CBF 60 min after loading dosage (20 mg/kg i.v.). Likewise, no significant change in mean arterial blood pressure, heart rate or transcutaneous gas tensions was observed. Though slight changes in CBF of short duration cannot be excluded, conventional dosage of phenobarbital to term newborn infants with foetal distress apparently imposes no risk of cerebrovascular damage.
    Type of Medium: Electronic Resource
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