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Titolo:
GD3 synthase gene expression in PC12 cells results in the continuous activation of TrkA and ERK1/2 and enhanced proliferation
Autore:
Fukumoto, S; Mutoh, T; Hasegawa, T; Miyazaki, H; Okada, M; Goto, G; Furukawa, K; Urano, T; Furukawa, K;
Indirizzi:
Nagoya Univ, Sch Med, Dept Biochem 2, Showa Ku, Nagoya, Aichi 4660065, Japan Nagoya Univ Nagoya Aichi Japan 4660065 a Ku, Nagoya, Aichi 4660065, Japan Fukui Med Sch, Dept Internal Med 2, Fukui 9101193, Japan Fukui Med Sch Fukui Japan 9101193 t Internal Med 2, Fukui 9101193, Japan Nagasaki Univ, Sch Dent, Dept Pediat Dent, Nagasaki 8528588, Japan Nagasaki Univ Nagasaki Japan 8528588 ediat Dent, Nagasaki 8528588, Japan Nagasaki Univ, Sch Med, Dept Pediat, Nagasaki 8528588, Japan Nagasaki Univ Nagasaki Japan 8528588 ept Pediat, Nagasaki 8528588, Japan Hokkaido Univ, Sch Dent, Dept Pediat Dent, Sapporo, Hokkaido 0608586, Japan Hokkaido Univ Sapporo Hokkaido Japan 0608586 oro, Hokkaido 0608586, Japan
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 8, volume: 275, anno: 2000,
pagine: 5832 - 5838
SICI:
0021-9258(20000225)275:8<5832:GSGEIP>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVE GROWTH-FACTOR; GANGLIOSIDE-MEDIATED MODULATION; NEURONAL DIFFERENTIATION; RAT-BRAIN; TYROSINE PHOSPHORYLATION; PHEOCHROMOCYTOMA CELLS; MONOCLONAL-ANTIBODIES; RECEPTOR FUNCTION; LEUKEMIA-CELLS; HUMAN-MELANOMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Furukawa, K Nagoya Univ, Sch Med, Dept Biochem 2, Showa Ku, 65 Tsurumai, Nagoya, Aichi4660065, Japan Nagoya Univ 65 Tsurumai Nagoya Aichi Japan 4660065 0065, Japan
Citazione:
S. Fukumoto et al., "GD3 synthase gene expression in PC12 cells results in the continuous activation of TrkA and ERK1/2 and enhanced proliferation", J BIOL CHEM, 275(8), 2000, pp. 5832-5838

Abstract

A rat pheochromocytoma cell line (PC12) transfected with ganglioside GD3 synthase gene showed a marked change in the ganglioside profile and enhancedproliferation and no response of neurite extension to nerve growth factor (NGF) stimulation. In these transfectant cells, a continuous phosphorylation of TrkA and the activation of ERK1/2 without NGF treatment were observed. Proliferation inhibition experiments with kinase inhibitors such as herbimycin A, K-252a, and PD98059 revealed that the enhanced proliferation was actually due to the activation of the Ras/MEK/ERK pathway. A TrkA dimer was detected in the GD3 synthase transfectant cells regardless of NGF treatment by crosslinking and immunoblotting, The increased expression of GD1b and GT1b in these transfectant cells might induce the conformational change of TrkA to form a dimer and to be activated continuously, These results may indicate regulatory roles of gangliosides in cell proliferation under physiological and malignant processes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 02:16:46