v-erbA specifically suppresses transcription of the avian erythrocyte anion transporter (Band 3) gene

The carbonic anhydrase I locus contains a c-Myb target promoter and modulates differentiation of murine erythroleukemia cells

“…However, v-Erb-A is able to confer pH and salt tolerance to v-Erb-B-transformed erythroblasts and appears to prevent their spontaneous differentiation. v-ErbA is postulated to contribute to erythroleukemia by repression of erythroid-specific genes (Zenke et al, 1988;Disela et al, 1991;), which include CAII and Band 3 (erythrocyte H þ /Na þ exchanger) (Ciana et al, 1998). Both CAII and Band 3 are expressed at low levels in primary avian erythroblasts and are not detectable in MEL cells.…”

The fibroblast growth factor receptor FGFR-4 acts as a ligand dependent modulator of erythroid cell proliferation

“…Brie¯y, following Ficoll-Hypaque centrifugation (density 1.077 g/cm 3 , Eurobio, Paris, France) bone marrow cells were cultured in modi®ed CFU-E medium (2 ± 4610 6 cells/ml; Radke et al, 1982;Zenke et al, 1988;Beug et al, 1995) containing 100 ng/ ml avian SCF (Hayman et al, 1993;Bartunek et al, 1996). Recombinant chicken myelomonocytic growth factor (cMGF, 40 ng/ml; Leutz et al, 1984;Bartunek et al, 1996Bartunek et al, , 1997 was present during the initial phase of culture (day 1 and 2) to induce di erentiation and adherence of macrophages and macrophage precursor cells.…”

“…To induce erythroid di erentiation, cultures of SCF and TGFa progenitors (2610 6 cells/ml) were incubated in CFU-E medium without chicken serum (referred to as di erentiation medium; Zenke et al, 1988) supplemented with 5% anemic chicken serum (as a source for Epo) and 1 mg/ml recombinant human insulin (Novo Nordisk). CEA-HD3 erythroblasts were induced to di erentiate by temperature shift to 428C in di erentiation medium plus anemic chicken serum and insulin as above; cells were treated with 10 77 M T3 to activate the c-erbA/TR or left untreated (Zenke et al, 1988;Disela et al, 1991).…”

“…CEA-HD3 erythroblasts were induced to di erentiate by temperature shift to 428C in di erentiation medium plus anemic chicken serum and insulin as above; cells were treated with 10 77 M T3 to activate the c-erbA/TR or left untreated (Zenke et al, 1988;Disela et al, 1991).…”

The Evi-1 proto-oncogene encodes a transcriptional repressor activity associated with transformation

“…Evi-1 also has a transcriptional repressor activity that is required for transformation in addition to the previously described trans-activation function (Morishita et al, 1995). Several interesting possibilities exist for the potential physiological targets of transcriptional repressors which would contribute to tumourigenesis, including repression of: (1) a limited group of tissue speci®c genes, as for the erythroid and myeloid speci®c genes regulated by v-erbA (Zenke et al, 1988) and AML1B (Zhang et al, 1994) respectively; (2) key transcriptional control factors, eg GATA, SCL MYB, AML1 and PU.1, regulating haematopoietic development (Shivdasani and Orkin, 1996); (3) negative regulators of cell proliferation such as the cyclin-dependent kinase inhibitors p15INK4A, p16INK4B, p21 and p27 (Hirama and Koe er, 1995) and (4) negative regulators of apoptosis such as the Bcl-2 antagonists Bax (Oltvai et al, 1993) and Bcl-X (Boise et al, 1993). Clearly, selective suppression of gene expression might play a key role in Evi-1 mediated leukaemogenesis.…”