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X-linked inhibitor of apoptosis (XIAP) protein protects against caspase activation and tissue loss after neonatal hypoxia-ischemia

Journal article
Authors Xiaoyang Wang
Changlian Zhu
X Wang
Henrik Hagberg
L. Korhonen
Mats Sandberg
D. Lindholm
Klas Blomgren
Published in Neurobiol Dis
Volume 16
Issue 1
Pages 179-89
Publication year 2004
Published at Institute for the Health of Women and Children, Dept of Obstetrics and Gynaecology
Institute of Physiology and Pharmacology, Dept of Medical Biophysics
Institute for the Health of Women and Children, Dept of Paediatrics
Institute of Physiology and Pharmacology, Dept of Physiology
Pages 179-89
Language en
Keywords Animals, Animals, Newborn, *Apoptosis/genetics, Caspases/genetics/*metabolism, Comparative Study, Enzyme Activation/genetics, Female, Humans, Hypoxia-Ischemia, Brain/enzymology/genetics/*metabolism/*pathology, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Protein Biosynthesis, Proteins/genetics/*physiology, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., X-Linked Inhibitor of Apoptosis Protein
Subject categories Experimental brain research, Neurobiology


Nine-day-old transgenic XIAP overexpressing (TG-XIAP) and wild-type mice were subjected to left carotid artery ligation and 10% O(2) for 60 min, leading to widespread infarctions in the ipsilateral hemisphere during reperfusion. The activation of caspase-3 and -9 seen in wild-type animals was virtually abolished in TG-XIAP mice. Tissue loss was significantly reduced from 54.4 +/- 4.1 mm(3) (mean +/- SEM) in wild-type mice to 33.1 +/- 2.1 mm(3) in the TG-XIAP mice. Injured neurons displayed stronger XIAP staining during reperfusion, particularly in the nuclei. XIAP was colocalized with XAF-1, Smac, and HtrA2 in injured neurons after hypoxia-ischemia (HI). XIAP was cleaved after HI, and Smac immunoprecipitation co-precipitated a 25-kDa C-terminal fragment of XIAP, indicating that Smac preferentially bound to cleaved XIAP. These findings provide the first evidence that increased XIAP levels protect the neonatal brain against HI.

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