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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Wulf Paschen

Max-Planck-Institute for Neurological Research

Department of Experimental Neurology




Name/email consistency: high



  • Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany. 1998 - 2004
  • Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Germany. 2000 - 2004


  1. Brain trauma induces X-box protein 1 processing indicative of activation of the endoplasmic reticulum unfolded protein response. Paschen, W., Yatsiv, I., Shoham, S., Shohami, E. J. Neurochem. (2004) [Pubmed]
  2. GADD34 protein levels increase after transient ischemia in the cortex but not in the CA1 subfield: implications for post-ischemic recovery of protein synthesis in ischemia-resistant cells. Paschen, W., Hayashi, T., Saito, A., Chan, P.H. J. Neurochem. (2004) [Pubmed]
  3. Endoplasmic reticulum dysfunction in brain pathology: critical role of protein synthesis. Paschen, W. Current. Neurovascular. Research (2004) [Pubmed]
  4. Transient cerebral ischemia activates processing of xbp1 messenger RNA indicative of endoplasmic reticulum stress. Paschen, W., Aufenberg, C., Hotop, S., Mengesdorf, T. J. Cereb. Blood Flow Metab. (2003) [Pubmed]
  5. Shutdown of translation: lethal or protective? Unfolded protein response versus apoptosis. Paschen, W. J. Cereb. Blood Flow Metab. (2003) [Pubmed]
  6. Mechanisms of neuronal cell death: diverse roles of calcium in the various subcellular compartments. Paschen, W. Cell. Calcium (2003) [Pubmed]
  7. Endoplasmic reticulum: a primary target in various acute disorders and degenerative diseases of the brain. Paschen, W. Cell. Calcium (2003) [Pubmed]
  8. Conditions associated with ER dysfunction activate homer 1a expression. Paschen, W., Mengesdorf, T. J. Neurochem. (2003) [Pubmed]
  9. Dependence of vital cell function on endoplasmic reticulum calcium levels: implications for the mechanisms underlying neuronal cell injury in different pathological states. Paschen, W. Cell. Calcium (2001) [Pubmed]
  10. Peroxidative stress selectively down-regulates the neuronal stress response activated under conditions of endoplasmic reticulum dysfunction. Paschen, W., Mengesdorf, T., Althausen, S., Hotop, S. J. Neurochem. (2001) [Pubmed]
  11. Endoplasmic reticulum dysfunction--a common denominator for cell injury in acute and degenerative diseases of the brain?. Paschen, W., Frandsen, A. J. Neurochem. (2001) [Pubmed]
  12. Effect of transient focal ischemia of mouse brain on energy state and NAD levels: no evidence that NAD depletion plays a major role in secondary disturbances of energy metabolism. Paschen, W., Oláh, L., Mies, G. J. Neurochem. (2000) [Pubmed]
  13. Role of calcium in neuronal cell injury: which subcellular compartment is involved?. Paschen, W. Brain Res. Bull. (2000) [Pubmed]
  14. Ischemia-induced changes in 2'-5'-oligoadenylate synthethase mRNA levels in rat brain: comparison with changes produced by perturbations of endoplasmic reticulum calcium homeostasis in neuronal cell cultures. Paschen, W., Althausen, S., Doutheil, J. Neurosci. Lett. (1999) [Pubmed]
  15. Erp72 expression activated by transient cerebral ischemia or disturbance of neuronal endoplasmic reticulum calcium stores. Paschen, W., Gissel, C., Linden, T., Doutheil, J. Metab. Brain. Dis (1998) [Pubmed]
  16. Effects of transient cerebral ischemia on hsp40 mRNA levels in rat brain. Paschen, W., Linden, T., Doutheil, J. Brain Res. Mol. Brain Res. (1998) [Pubmed]
  17. Activation of gadd153 expression through transient cerebral ischemia: evidence that ischemia causes endoplasmic reticulum dysfunction. Paschen, W., Gissel, C., Linden, T., Althausen, S., Doutheil, J. Brain Res. Mol. Brain Res. (1998) [Pubmed]
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