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141. Norman, M. U., James, W. G. & Hickey, M. J. (2008) Differential roles of ICAM-1
and VCAM-1 in leukocyte-endothelial cell interactions in skin and brain of MRL/
faslpr mice. J. Leukoc. Biol. 84: 68-76.
142. Takeda, H., Spatz, M., Ruetzler, C., McCarron, R., Becker, K. & Hallenbeck, J.
(2002) Induction of mucosal tolerance to E-selectin prevents ischemic and hemor-
rhagic stroke in spontaneously hypertensive genetically stroke-prone rats. Stroke
33: 2156-2163.
143. Lipton, P. (1999) Ischemic cell death in brain neurons. Physiol. Rev. 79: 1431-
1568.
144. Danton, G. H. & Dietrich, W. D. (2003) Inflammatory mechanisms after ischemia
and stroke. J. Neuropathol. Exp. Neurol. 62: 127-136.
145. Deng, L., Wang, C., Spencer, E., Yang, L., Braun, A., You, J., Slaughter, C., Pickart,
C. & Chen, Z. J. (2000) Activation of the IkappaB kinase complex by TRAF6
requires a dimeric ubiquitin-conjugating enzyme complex and a unique polyubiq-
uitin chain. Cell 103: 351-361.
146. Williams, A. J., Berti, R., Dave, J. R., Elliot, P. J., Adams, J. & Tortella, F. C. (2004)
Delayed treatment of ischemia/reperfusion brain injury: extended therapeutic
window with the proteosome inhibitor MLN519. Stroke 35: 1186-1191.
147. Williams, A. J., Dave, J. R. & Tortella, F. C. (2006) Neuroprotection with the pro-
teasome inhibitor MLN519 in focal ischemic brain injury: relation to nuclear
factor kappaB (NF-kappaB), inflammatory gene expression, and leukocyte infil-
tration. Neurochem. Int. 49: 106-112.
148. Phillips, J. B., Williams, A. J., Adams, J., Elliott, P. J. & Tortella, F. C. (2000) Protea-
some inhibitor PS519 reduces infarction and attenuates leukocyte infiltration in
a rat model of focal cerebral ischemia. Stroke 31: 1686-1693.
149. Williams, A. J., Hale, S. L., Moffett, J. R., Dave, J. R., Elliott, P. J., Adams, J. &
Tortella, F. C. (2003) Delayed treatment with MLN519 reduces infarction and
associated neurologic deficit caused by focal ischemic brain injury in rats via
antiinflammatory mechanisms involving nuclear factor-kappaB activation, gliosis,
and leukocyte infiltration. J. Cereb. Blood Flow Metab. 23: 75-87.
150. Cookson, M. R., Menzies, F. M., Manning, P., Eggett, C. J., Figlewicz, D. A., McNeil,
C. J. & Shaw, P. J. (2002) Cu/Zn superoxide dismutase (SOD1) mutations associ-
ated with familial amyotrophic lateral sclerosis (ALS) affect cellular free radical
release in the presence of oxidative stress. Amyotroph. Lateral Scler. Other Motor
Neuron Disord. 3: 75-85.
151. Jaiswal, M. K. & Keller, B. U. (2009) Cu/Zn superoxide dismutase typical for
familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria
and perturbs Ca2+ homeostasis in SOD1G93A mice. Mol. Pharmacol. 75: 478-
489.
152. Kabashi, E. & Durham, H. D. (2006) Failure of protein quality control in amyo-
trophic lateral sclerosis. Biochim. Biophys. Acta 1762: 1038-1050.
153. Kato, S., Horiuchi, S., Liu, J., Cleveland, D. W., Shibata, N., Nakashima, K., Nagai,
R., Hirano, A., Takikawa, M. et al. (2000) Advanced glycation endproduct-modified
superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyo-
trophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice
expressing human SOD1 with a G85R mutation. Acta Neuropathol. 100: 490-
505.
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