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Titolo:
Regulation of Id2 gene expression by the type 1 IGF receptor and the insulin receptor substrate-1
Autore:
Navarro, M; Valentinis, B; Belletti, B; Romano, G; Reiss, K; 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: 12, volume: 142, anno: 2001,
pagine: 5149 - 5157
SICI:
0013-7227(200112)142:12<5149:ROIGEB>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOOP-HELIX PROTEIN; GROWTH-FACTOR-I; PLECKSTRIN HOMOLOGY; HEMATOPOIETIC-CELLS; S6 KINASE; INSULIN-LIKE-GROWTH-FACTOR-1 RECEPTOR; PHOSPHATIDYLINOSITOL 3-KINASE; GRANULOCYTIC DIFFERENTIATION; RETINOBLASTOMA PROTEIN; SIGNALING PATHWAYS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Baserga, R Thomas Jefferson Univ, Kimmel Canc Ctr, 233 S 10th St, Philadelphia, PA 19107 USA Thomas Jefferson Univ 233 S 10th St Philadelphia PA USA 19107 A
Citazione:
M. Navarro et al., "Regulation of Id2 gene expression by the type 1 IGF receptor and the insulin receptor substrate-1", ENDOCRINOL, 142(12), 2001, pp. 5149-5157

Abstract

The Id family of helix-loop-helix proteins is known to be involved in the proliferation and differentiation of several types of cells. The type I IGFreceptor (IGF-IR) induces either proliferation or differentiation in 32D cells, a murine hemopoietic cell line, depending on the availability of the appropriate substrates for the receptor. We have previously reported that the IGF-IR regulates the expression of the Id2 gene in 32D cells. We now show that the IGF-IR controls the increase in Id2 gene expression through at least three pathways. These three pathways originate from the tyrosine residue at 950, a domain in the C-terminus, and the activation of the insulin receptor substrate-l (IRS-1) by the receptor. IRS-1 is the preponderant signal, and its effect on Id2 gene expression requires a functional phosphotyrosine binding domain. With wild-type IRS-1, Id2 gene expression is increased,even in those cells that express IGF-I receptors defective in Id2 signaling. Rapamycin, an inhibitor of p70(S6K), a downstream effector of IRS-1 signaling, partially inhibits (but does not completely abrogate) the increase in Id2 gene expression. A mutant IRS-1 with a deletion of the Pleckstrin domain is as effective as wild-type IRS-1 in up-regulating Id2 gene expression. In addition, it seems to increase the stability of p70(S6K). Our results indicate that the IGF-IR regulates Id2 gene expression through different pathways. At least in 32D cells, increased Id2 gene expression seems to correlate more with inhibition of differentiation than with proliferation.

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Documento generato il 01/12/20 alle ore 01:12:29