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Titolo:
Regulation of X-chromosome-linked inhibitor of apoptosis protein in kainicacid-induced neuronal death in the rat hippocampus
Autore:
Korhonen, L; Belluardo, N; Lindholm, D;
Indirizzi:
Univ Uppsala, Ctr Biomed, Dept Neurosci, S-75123 Uppsala, Sweden Univ Uppsala Uppsala Sweden S-75123 pt Neurosci, S-75123 Uppsala, Sweden Univ Palermo, Fac Med, Inst Human Physiol, I-95125 Palermo, Italy Univ Palermo Palermo Italy I-95125 Human Physiol, I-95125 Palermo, Italy
Titolo Testata:
MOLECULAR AND CELLULAR NEUROSCIENCE
fascicolo: 2, volume: 17, anno: 2001,
pagine: 364 - 372
SICI:
1044-7431(200102)17:2<364:ROXIOA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; DEPENDENT REGULATION; MESSENGER-RNAS; GENE; EXPRESSION; FAMILY; BRAIN; XIAP; NAIP; IAP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Lindholm, D Univ Uppsala, Ctr Biomed, Dept Neurosci, Box 587, S-75123 Uppsala, Sweden Univ Uppsala Box 587 Uppsala Sweden S-75123 3 Uppsala, Sweden
Citazione:
L. Korhonen et al., "Regulation of X-chromosome-linked inhibitor of apoptosis protein in kainicacid-induced neuronal death in the rat hippocampus", MOL CELL NE, 17(2), 2001, pp. 364-372

Abstract

XIAP (X-chromosome-linked inhibitor of apoptosis protein) is an antiapoptotic protein which inhibits the activity of caspases and suppresses cell death. However, little is known about the presence and function of XIAP in thenervous system. Here we report that XIAP mRNA is expressed in developing and adult rat brain. Using a specific antibody, we observed XIAP-immunoreactive cells in different brain regions, among others, in the hippocampus and cerebral cortex. Kainic acid, which induces delayed cell death of specific neurons, increased the levels of XIAP in the CA3 region of hippocampus. XIAP was, however, largely absent in cells undergoing cell death, as shown by TUNEL labeling and staining for active caspase-3. In cultured hippocampal neurons, XIAP was initially upregulated by kainic acid and then degraded in a process blocked by the caspase-3 inhibitor DEVD. Similarly, recombinant XIAP is cleaved by active caspase-3 in vitro. The results show that there isbiphasic regulation of XIAP in the hippocampus following kainic acid and that XIAP becomes a target for caspase-3 activated during cell death in the hippocampus. The degradation of XIAP by kainic acid contributes to neuronalcell death observed in vulnerable neurons of the hippocampus after caspaseactivation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 09:13:30