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Titolo:
Domains of the insulin-like growth factor I receptor required for the activation of extracellular signal-regulated kinases
Autore:
Dews, M; Prisco, M; Peruzzi, F; Romano, G; Morrione, A; Baserga, R;
Indirizzi:
Thomas Jefferson Univ, Kimmel Canc Ctr, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA
Titolo Testata:
ENDOCRINOLOGY
fascicolo: 4, volume: 141, anno: 2000,
pagine: 1289 - 1300
SICI:
0013-7227(200004)141:4<1289:DOTIGF>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
IGF-I; INSULIN-LIKE-GROWTH-FACTOR-1 RECEPTOR; PHOSPHATIDYLINOSITOL 3'-KINASE; TYROSINE KINASE; TRANSFORMING ACTIVITIES; NUCLEAR TRANSLOCATION; HEMATOPOIETIC-CELLS; MAP KINASES; SUBSTRATE-1; APOPTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Baserga, R Thomas Jefferson Univ, Kimmel Canc Ctr, 233 S 10th St,624 BLSB,Philadelphia, PA 19107 USA Thomas Jefferson Univ 233 S 10th St,624 BLSB Philadelphia PA USA 19107
Citazione:
M. Dews et al., "Domains of the insulin-like growth factor I receptor required for the activation of extracellular signal-regulated kinases", ENDOCRINOL, 141(4), 2000, pp. 1289-1300

Abstract

The type 1 insulin-like growth factor receptor (IGF-IR) activates the extracellular signal-regulated kinases (ERK1 and -2). The two major substrates of the IGF-IR, insulin receptor substrate-1 (IRS-1) and the She proteins, are known to contribute to this activation. We investigated the domains of the IGF-IR required for the activation of the ERK proteins. To facilitate this study, rye used a cell line (32D cells) that lacks IRS-1. In the absenceof IRS-1, ERK activation is inhibited if the IGF-IR is mutated at two domains: tyrosine Y950 and a serine quartet at 1280-1283. Expression of IRS-1 in 32D cells expressing the double mutant IGF-IR restores ERK activation. The importance of the C-terminus of the IGF-IR in ERK activation (in the absence of IRS-1) is confirmed by the failure of the insulin receptor to give asustained activation of ERK. In this model system, there is a good, but not exact, correlation between ERK activation and cell survival after withdrawal of growth factors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 09:47:31