Cell-specific regulation of the c-myc gene by lymphocyte mitogens and platelet-derived growth factor

c-Myc-deficient B lymphocytes are resistant to spontaneous and induced cell death

“…[1][2][3][4][5] One of its members, c-Myc, is expressed from immature stages of B-cell differentiation, and is rapidly induced upon mitogenic stimulation. [6][7][8] Overexpression of c-myc induces apoptosis in fibroblasts and myeloid cell lines in low serum conditions. 1,2,9 More recently, Hueber et al 10 have shown that c-Myc-induced apoptosis in fibroblasts requires the interaction on the cell surface of CD95, a member of the TNF receptor family, and its ligand CD95L, triggering an apoptotic pathway that activates a set of cysteine proteases, called caspases, which lead to cell death.…”

A genetic screen to identify genes that rescue the slow growth phenotype of c-myc null fibroblasts

“…c-Myc expression is induced upon mitogenic signaling and peaks 3 ± 4 h after growth factor stimulation (Kelly et al, 1983). In cycling cells, c-Myc levels remain invariant and decline after induction of di erentiation (Einat et al, 1985;Pietenpol et al, 1990).…”

Repression of c-Myc responsive genes in cycling cells causes G1 arrest through reduction of cyclin E/CDK2 kinase activity

“…Myc expression is activated by mitogenic signals (Kelly et al, 1983) and is suppressed by growth-inhibitory signals (Einat et al, 1985;Pietenpol et al, 1990;Alexandrow et al, 1995), but is invariant in exponentially growing cells (Hann et al, 1985;Thompson et al, 1986). Activation of c-myc is su cient to induce cell cycle entry in quiescent cells (Eilers et al, 1991).…”