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Titolo:
Calcium/calmodulin-dependent protein kinase inhibition potentiates thapsigargin-mediated cell death in SH-SY5Y human neuroblastoma cells
Autore:
McGinnis, KM; Wang, KKW; Gnegy, ME;
Indirizzi:
Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 t Pharmacol, Ann Arbor, MI 48109 USA Warner Lambert Co, Parke Davis Pharmaceut Res Div, Lab Neurobiochem, Dept Neurosci Therapeut, Ann Arbor, MI 48105 USA Warner Lambert Co Ann Arbor MIUSA 48105 erapeut, Ann Arbor, MI 48105 USA
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 2, volume: 301, anno: 2001,
pagine: 99 - 102
SICI:
0304-3940(20010330)301:2<99:CPKIPT>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEURONAL APOPTOSIS; IV; PHOSPHORYLATION; CALPAIN; KN-93; ICE;
Keywords:
apoptosis; Ca2+/CaM-dependent protein kinase; caspase-3; KN93; k252a; SH-SY5Y cells; thapsigargin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
16
Recensione:
Indirizzi per estratti:
Indirizzo: Gnegy, ME Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 l, Ann Arbor, MI 48109 USA
Citazione:
K.M. McGinnis et al., "Calcium/calmodulin-dependent protein kinase inhibition potentiates thapsigargin-mediated cell death in SH-SY5Y human neuroblastoma cells", NEUROSCI L, 301(2), 2001, pp. 99-102

Abstract

We previously demonstrated a loss in Ca2+/Calmodulin-dependent protein kinase (CaM kinase) activity in SH-SY5Y undergoing thapsigargin-mediated apoptosis. To extend that finding we report that CaM kinase inhibition potentiates thapsigargin-mediated cell death. CaM kinase inhibitor KN93 on its own exhibits little toxicity up to 10 mM, as measured by release of lactate dehydrogenase (LDH) into the culture medium. In SH-SY5Y cells pretreated with KN93 and the nonselective protein ki nase inhibitor k252a and then treated with 2 m M thapsigargin, loss of viability is significantly greater than in cells treated with thapsigargin alone, Pretreatment with the pan-caspase inhibitor Z-D-DCB prevented the thapsigargin-mediated increase in LDH release. Furthermore, thapsigargin-induced caspase-3-like activation, demonstratedby poly(ADP)ribose polymerase cleavage and pro-caspase-3 processing, was elevated in the presence of KN93. (C) 2001 Elsevier Science Ireland Ltd. Allrights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 09:22:15