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Titolo:
The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation
Autore:
Cole, MD; McMahon, SB;
Indirizzi:
Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA Princeton Univ Princeton NJ USA 08544 t Mol Biol, Princeton, NJ 08544 USA
Titolo Testata:
ONCOGENE
fascicolo: 19, volume: 18, anno: 1999,
pagine: 2916 - 2924
SICI:
0950-9232(19990513)18:19<2916:TMOACE>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN C-MYC; YEAST TRANSCRIPTIONAL ACTIVATORS; HISTONE DEACETYLASE ACTIVITY; TRANSFORM NORMAL-CELLS; TATA-BINDING PROTEIN; DNA-BINDING; E-BOX; NEOPLASTIC TRANSFORMATION; ORNITHINE DECARBOXYLASE; IN-VIVO;
Keywords:
Myc; oncoprotein; target gene; transactivation; chromatin remodelling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
85
Recensione:
Indirizzi per estratti:
Indirizzo: Cole, MD Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA Princeton Univ Princeton NJ USA 08544 l, Princeton, NJ 08544 USA
Citazione:
M.D. Cole e S.B. McMahon, "The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation", ONCOGENE, 18(19), 1999, pp. 2916-2924

Abstract

Mutations which disrupt the regulation or expression level of the c-myc gene are among the most common found in human and animal cancers (reviewed inref. Cole, 1986; Henriksson and Luscher, 1996; Marcu et al., 1992). Ectopic expression studies define numerous biological activities of the c-myc gene, including transformation, immortalization? blockage of cell differentiation and induction of apoptosis (Askew et al., 1991; Cole, 1986; Evan and Littlewood, 1993; Freytag et al., 1990; Henriksson and Luscher, 1996; Marcu et al., 1992). Furthermore, c-myc is required for efficient progression through the cell cycle (Goruppi et al., 1994; Prochownik et al., 1988; Yokoyamaand Imamoto, 1987), although recent studies indicate that it is not absolutely essential (Mateyak et al., 1997). This fascinating array of biologicalactivities makes the c-myc gene one of the most intriguing oncogenes and presents the challenging question of how a single gene can manifest so many different effects. The c-Myc protein exhibits sequence-specific DNA bindingwhen dimerized with its partner Max, and DNA binding is mediated through the basic region, which recognizes the core sequence CACGTG (Berberich et al., 1992; Blackwell et al., 1993; Blackwood and Eisenman, 1991; Prendergast and Ziff, 1991; Prendergast et al., 1991), but exhibits somewhat higher affinity for the more extended sequence ACCACGTGGT (Berberich et al., 1992; Blackwell et al., 1993; Halazonetis and Kandil, 1991). There are three closely related Myc family proteins (c-Myc, N-Myc and L-Myc), each with documented oncogenic potential (Birrer et al., 1988; Schwab et al., 1985; Yancopoulos et al., 1985) and similar DNA binding properties (Mukherjee et al., 1992). For simplicity, we will use the term Myc to refer to all three proteins, but delineate any distinct activities where they apply. The goal of this review is to discuss Myc as a transcriptional activator and critically evaluate the evidence for the transactivation of specific target genes as direct downstream effecters. Since excellent comprehensive reviews on Myc have been published recently (Facchini and Penn, 1998; Henriksson and Luscher, 1996), we will focus on the latest observations that offer mechanistic insight into transactivation and oncogenic transformation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/01/21 alle ore 23:14:56