Glutathione peroxidase 4 senses and translates oxidative stress into 12/15-lipoxygenase dependent- and AIF-mediated cell death.
- A. Seiler, Manuela Schneider, M. Conrad
- BiologyCell Metabolism
- 3 September 2008
Reactive glia in the injured brain acquire stem cell properties in response to sonic hedgehog. [corrected].
- S. Sirko, Gwendolyn Behrendt, M. Götz
- BiologyCell Stem Cell
- 4 April 2013
Shrinkage-mediated imaging of entire organs and organisms using uDISCO
- Chenchen Pan, Ruiyao Cai, Ali Ertürk
- BiologyNature Methods
- 22 August 2016
The 'ultimate DISCO' (uDISCO) clearing is developed to overcome limitations in volumetric imaging and preserves fluorescent proteins over months and renders intact organs and rodent bodies transparent while reducing their size up to 65%.
BID mediates neuronal cell death after oxygen/ glucose deprivation and focal cerebral ischemia
- N. Plesnila, S. Zinkel, M. Moskowitz
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 11 December 2001
The findings suggest that BID and the mitochondrial-amplification pathway promoting caspase activation contributes importantly to neuronal cell death after ischemic insult.
Apoptosis-Inducing Factor Triggered by Poly(ADP-Ribose) Polymerase and Bid Mediates Neuronal Cell Death after Oxygen-Glucose Deprivation and Focal Cerebral Ischemia
- C. Culmsee, Changlian Zhu, N. Plesnila
- BiologyJournal of Neuroscience
- 2 November 2005
Results provide the first evidence for a causal role of AIF in ischemic neuronal cell death and suggest caspase-independent cell death signaling may provide a promising novel target for therapeutic interventions in cerebrovascular diseases.
High cortical spreading depression susceptibility and migraine‐associated symptoms in Cav2.1 S218L mice
- A. M. van den Maagdenberg, T. Pizzorusso, M. Ferrari
- Biology, MedicineAnnals of Neurology
- 1 January 2010
The CACNA1A gene encodes the pore‐forming subunit of neuronal CaV2.1 Ca2+ channels that causes a dramatic hemiplegic migraine syndrome that is associated with ataxia, seizures, and severe, sometimes fatal, brain edema often triggered by only a mild head trauma.
Bid-induced release of AIF from mitochondria causes immediate neuronal cell death
- S. Landshamer, M. Hoehn, C. Culmsee
- Biology, ChemistryCell Death and Differentiation
- 6 June 2008
Bid-mediated mitochondrial release of AIF followed by rapid nuclear translocation is a major mechanism of glutamate-induced neuronal death.
Delayed neuronal death after brain trauma involves p53-dependent inhibition of NF-κB transcriptional activity
- N. Plesnila, L. Baumgarten, C. Culmsee
- Biology, ChemistryCell Death and Differentiation
- 1 August 2007
Delayed neuronal cell death after brain trauma is mediated by p53-dependent mechanisms that involve inhibition of NF-κB transcriptional activity, and p53 inhibition provides a promising approach for the treatment of acute brain injury.
Inhibition of Drp1 provides neuroprotection in vitro and in vivo
- J. Grohm, S. Kim, C. Culmsee
- BiologyCell Death and Differentiation
- 2 March 2012
Investigation of the role of dynamin-related protein 1 (Drp1) in neuronal cell death induced by glutamate toxicity or oxygen–glucose deprivation in vitro, and after ischemic brain damage in vivo indicates that Drp1 translocation and associated mitochondrial fission are key features preceding the loss of MMP and neuronal cellDeath.
Experimental Subarachnoid Hemorrhage Causes Early and Long-Lasting Microarterial Constriction and Microthrombosis: An in-vivo Microscopy Study
- B. Friedrich, Frank Müller, S. Feiler, K. Schöller, N. Plesnila
- Medicine, BiologyJournal of Cerebral Blood Flow and Metabolism
- 1 March 2012
It is demonstrated that SAH induces microarterial constrictions and microthrombosis in vivo, which may explain the early CPP-independent decrease in cerebral blood flow after SAH and may therefore serve as novel targets for the treatment of early perfusion deficits afterSAH.
...
...