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Titolo:
Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury
Autore:
Springer, JE; Azbill, RD; Nottingham, SA; Kennedy, SE;
Indirizzi:
Univ Kentucky, Med Ctr, Dept Anat & Neurobiol, Ctr Spinal Cord & Brain Injury Res, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 Injury Res, Lexington, KY 40536 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 19, volume: 20, anno: 2000,
pagine: 7246 - 7251
SICI:
0270-6474(20001001)20:19<7246:CBDATC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXCITATORY AMINO-ACIDS; CYTOCHROME-C; BRAIN INJURY; CELL-DEATH; MITOCHONDRIAL-FUNCTION; NEURONAL APOPTOSIS; CEREBRAL-ISCHEMIA; CYCLOSPORINE-A; PROTEIN; KINASE;
Keywords:
calcineurin; caspase-3; FK506; glutamate receptors; NMDA; Bcl-xL; BAD translocation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Springer, JE Univ Kentucky, Med Ctr, Dept Anat & Neurobiol, Ctr Spinal Cord & Brain Injury Res, 800 Rose St, Lexington, KY 40536 USA Univ Kentucky 800 Rose St Lexington KY USA 40536 KY 40536 USA
Citazione:
J.E. Springer et al., "Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury", J NEUROSC, 20(19), 2000, pp. 7246-7251

Abstract

We report here that activation of the caspase-3 apoptotic cascade in spinal cord injury is regulated, in part, by calcineurin-mediated BAD dephosphorylation. BAD, a proapoptotic member of the bcl-2 gene family, is rapidly dephosphorylated after injury, dissociates from 14-3-3 in the cytosol, and translocates to the mitochondria of neurons where it binds to Bcl-x(L). Pretreatment of animals with FK506, a potent inhibitor of calcineurin activity, or MK801, an NMDA glutamate receptor antagonist, blocked BAD dephosphorylation and abolished activation of the caspase-3 apoptotic cascade. These findings extend previous in vitro observations and are the first to implicate the involvement of glutamate-mediated calcineurin activation and BAD dephosphorylation as upstream, premitochondrial signaling events leading to caspase-3 activation in traumatic spinal cord injury.

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Documento generato il 24/11/20 alle ore 11:19:47