Reply to “Inhibition of post-ischemic brain injury by clusterin overexpression”
DM Holtzman, B Hee Han, YY He, GM Kim, J Choi… - Nature medicine, 2001 - nature.com
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877–884 (1994). 3. Han, BH et al. Clusterin contributes to caspase-3-independent brain
injury following neonatal hypoxia-ischemia. Nature Med. 7, 338–43 (2001). 4. De Bilbao, F.
et al. Cell death is prevented in thalamic fields but not in injured neocortical areas after
permanent focal ischaemia in mice overexpressing the anti-apoptotic protein Bcl-2. Eur J
Neurosci 12, 921–934 (2000).
injury following neonatal hypoxia-ischemia. Nature Med. 7, 338–43 (2001). 4. De Bilbao, F.
et al. Cell death is prevented in thalamic fields but not in injured neocortical areas after
permanent focal ischaemia in mice overexpressing the anti-apoptotic protein Bcl-2. Eur J
Neurosci 12, 921–934 (2000).
877–884 (1994). 3. Han, BH et al. Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia. Nature Med. 7, 338–43 (2001). 4. De Bilbao, F. et al. Cell death is prevented in thalamic fields but not in injured neocortical areas after permanent focal ischaemia in mice overexpressing the anti-apoptotic protein Bcl-2. Eur J Neurosci 12, 921–934 (2000).
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