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Titolo:
Necrotic cell death in C-elegans requires the function of calreticulin andregulators of Ca2+ release from the endoplasmic reticulum
Autore:
Xu, KL; Tavernarakis, N; Driscoll, M;
Indirizzi:
Rutgers State Univ, Dept Mol Biol & Biochem, Nelson Biol Labs, Piscataway,NJ 08855 USA Rutgers State Univ Piscataway NJ USA 08855 Labs, Piscataway,NJ 08855 USA
Titolo Testata:
NEURON
fascicolo: 6, volume: 31, anno: 2001,
pagine: 957 - 971
SICI:
0896-6273(20010927)31:6<957:NCDICR>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
CAENORHABDITIS-ELEGANS; DEPENDENT EXCITOTOXICITY; NEURONAL DEGENERATION; CORTICAL-NEURONS; CALCIUM; BRAIN; CHANNEL; GENES; NEURODEGENERATION; IDENTIFICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Driscoll, M Rutgers State Univ, Dept Mol Biol & Biochem, Nelson Biol Labs,A232,604 Allison Rd, Piscataway, NJ 08855 USA Rutgers State Univ A232,604 Allison Rd Piscataway NJ USA 08855
Citazione:
K.L. Xu et al., "Necrotic cell death in C-elegans requires the function of calreticulin andregulators of Ca2+ release from the endoplasmic reticulum", NEURON, 31(6), 2001, pp. 957-971

Abstract

In C. elegans, a hyperactivated MEC-4(d) ion channel induces necrotic-likeneuronal death that is distinct from apoptosis. We report that null mutations in calreticulin suppress both mec-4(d)-induced cell death and the necrotic cell death induced by expression of a constitutively activated Gas subunit. RNAi-mediated knockdown of calnexin, mutations in the ER Ca2+ release channels unc-68 (ryanodine receptor) or itr-1 (inositol 1,4,5 triphosphate receptor), and pharmacological manipulations that block ER Call release also suppress death. Conversely, thapsigargin-induced ER Ca2+ release can restore mec-4(d)-induced cell death when calreticulin is absent. We conclude that high [Ca2+](i) is a requirement for necrosis in C. elegans and suggest that an essential step in the death mechanism is release of ER-based Ca2+ stores. ER-driven Ca2+ release has previously been implicated in mammalian necrosis, suggesting necrotic death mechanisms may be conserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 11:54:50