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Sökning: WFRF:(Kavelaars Annemieke)

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  • Kavelaars, Annemieke, et al. (författare)
  • Stories in Molecular Medicine April 2021
  • 2021
  • Ingår i: Trends in Molecular Medicine. - : Elsevier. - 1471-4914 .- 1471-499X. ; 27:4, s. 293-296
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Life experiences influence our research and motivate us to ask scientific questions and shape research goals. Here, Trends in Molecular Medicine authors share their journey in science. Their portraits highlight the diversity of scientists and that there is no standard career in science. We hope that these inspiring stories will help to build bridges of understanding between science and society, and motivate others to join the melting pot of scientific disciplines united in Trends in Molecular Medicine.
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  • Nijboer, Cora H, et al. (författare)
  • Targeting the p53 pathway to protect the neonatal ischemic brain.
  • 2011
  • Ingår i: Annals of neurology. - : Wiley. - 1531-8249 .- 0364-5134.
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate whether inhibition of mitochondrial p53 association using pifithrin-μ (PFT-μ) represents a potential novel neuroprotective strategy to combat perinatal hypoxic-ischemic (HI) brain damage. METHODS: Seven-day-old rats were subjected to unilateral carotid artery occlusion and hypoxia followed by intraperitoneal treatment with PFT-μ, an inhibitor of p53 mitochondrial association or PFT-α an inhibitor of p53 transcriptional activity. Cerebral damage, sensorimotor and cognitive function, apoptotic pathways (cytosolic cytochrome c, Smac/DIABLO, active caspase 3), and oxidative stress (lipid peroxidation and PARP-1 cleavage) were investigated. RESULTS: PFT-μ treatment completely prevented the HI-induced increase in mitochondrial p53 association at 3 hours and reduced neuronal damage at 48 hours post-HI. PFT-μ had long-term (6-10 weeks post-HI) beneficial effects as sensorimotor and cognitive outcome improved and infarct size was reduced by ∼79%. Neuroprotection by PFT-μ treatment was associated with strong inhibition of apoptotic pathways and reduced oxidative stress. Unexpectedly, PFT-μ also inhibited HI-induced upregulation of p53 target genes. However, the neuroprotective effect of inhibiting only p53 transcriptional activity by PFT-α was significantly smaller and did not involve reduced oxidative stress. INTERPRETATION: We are the first to show that prevention of mitochondrial p53 association by PFT-μ strongly improves functional outcome and decreases lesion size after neonatal HI. PFT-μ not only inhibits mitochondrial release of cytochrome c, but also inhibits oxidative stress. We propose that as a consequence nuclear accumulation of p53 and transcription of proapoptotic target genes are prevented. In conclusion, targeting p53 mitochondrial association by PFT-μ may develop into a novel and powerful neuroprotective strategy. ANN NEUROL 2011;00:000-000.
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