v-erbA overexpression is required to extinguish c-erbA function in erythroid cell differentiation and regulation of the erbA target gene CAII.

Disela, Christine; Glineur, Corine; Bugge, Thomas H.; Sap, Jan; Stengl, Gabi; Dodgson, Jerry B.; Stunnenberg, Henk; Beug, Hartmut; Zenke, Martin

doi:10.1101/gad.5.11.2033

Cited by 80 publications

(88 citation statements)

References 53 publications

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“…Importantly, a clear downregulation of FGFR-4 transcripts was observed within 48 h of di erentiation for both TGFa and SCF cells. The same result was obtained in CEA-HD3 erythroblasts that ectopically express c-erbA/ thyroid hormone receptor (TR; Disela et al, 1991). Proliferating CEA-HD3 cells showed high expression levels of FGFR-4 that were reduced when cells were induced to di erentiate by temperature shift to 428C (Figure 5b).…”

Section: Expression Of Fgfr-4 Mrna Is Regulated During Erythroid DI Esupporting

confidence: 71%

“…However, so far murine (Disela et al, 1991) which were grown at 378C or induced to di erentiate at 428C in the absence or presence of thyroid hormone (T3) for various periods of time, as indicated. RNA blotting and hybridization were performed as in (a) FGFR-4 was found to lack mitogenic activity when ectopically expressed in BaF3 cells, while for example FGFR-1 assayed under the same conditions was active (Wang et al, 1994;Wang and Goldfarb, 1997).…”

Section: Bfgf Enhances the Proliferation Of Erythroid Progenitor Cellsmentioning

confidence: 99%

“…CEA ± HD3 erythroblasts ectopically expressing the cerbA/thyroid hormone receptor (TR) were grown at a density of 1610 6 cells/ml in CFU-E medium containing T3-depleted sera as described (Disela et al, 1991).…”

Section: Cells and Tissue Culturementioning

confidence: 99%

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

Bartůněk

Knespel

et al. 1999

Oncogene

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Receptor and non-receptor tyrosine kinases constitute a large family of proteins that play a pivotal role in hematopoiesis. Here we conducted a comprehensive survey of tyrosine kinase gene expression in primary erythroid progenitor cells from bone marrow by employing a PCR-based strategy that targets the conserved kinase encoding region. We demonstrate that erythroid progenitor cells express several receptor and nonreceptor tyrosine kinases, like c-kit, Jak1, Ryk, FAK, Syk, Arg, Csk and members of the insulin receptor family. Speci®c changes in the expression pro®le of tyrosine kinases were observed following di erentiation induction. We also report on the identi®cation of a new ligand dependent modulator of erythropoiesis, ®broblast growth factor receptor-4 (FGFR-4). FGFR-4 is e ectively expressed in erythroid progenitors and downregulated when cells di erentiate. Furthermore, the FGFR-4 ligand, basic ®broblast growth factor (bFGF), enhanced erythroid cell proliferation induced by SCF or insulin, and thus modulated both erythroid proliferation and di erentiation in vitro.

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Section: Expression Of Fgfr-4 Mrna Is Regulated During Erythroid DI Esupporting

confidence: 71%

Section: Bfgf Enhances the Proliferation Of Erythroid Progenitor Cellsmentioning

confidence: 99%

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

Bartůněk

Knespel

et al. 1999

Oncogene

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

2006

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“…First, v-erb A inhibits the liganded RAR and c-erb A transcriptional activity (Damm et al, 1989;Sap et al, 1989;Disela et al, 1991;Sande et al, 1993;Rascle et al, 1994). Di erent hypotheses have been proposed to account for the v-erb A antagonism.…”

Section: Introductionmentioning

confidence: 99%

Molecular basis of the cell-specific activity of v-erb A in quail myoblasts

et al. 1997

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We have previously shown that v-erb A expression strongly stimulates quail myoblast proliferation and di erentiation without alteration of the triiodothyronine (T3) in¯uence in this cell type. In order to understand the molecular basis of v-erb A action in myoblasts, we have studied the in¯uence of this oncoprotein on c-erb Aa1 encoded T3 nuclear receptor (TRa) activity. In transfection experiments, v-erb A did not inhibit the T3-dependent c-erb Aa1 transcriptional activity in QM7 myoblasts in contrast to its action in HeLa cells. However, it repressed the retinoic acid receptor RARa activity in both cell-types, indicating that v-erb A interactions with T3 or RA mediated transcription signi®cantly di ers. In EMSA experiments using a TRE pa1 probe, T3Ra binds as three complexes in HeLa cells. We have previously identi®ed the slow migrating complex, undetectable in QM7 myoblasts, as a T3R/ RXR heterodimer. Interestingly, v-erb A inhibited binding of this complex in HeLa cells, but did not a ect binding of the two other complexes in QM7 myoblasts. Expression of RXR (g isoform), the TRa dimerization partner absent in proliferating QM7 cells, restored inhibition of c-erb Aa1 transcriptional activity in these cells and abrogated the v-erb A myogenic in¯uence. Lastly, v-erb A induced a T3-independent cerb Aa1 activity in QM7 cells when cotransfected in equimolar ratio with the receptor, by inhibiting AP-1 activity and stimulating transcription of a reporter gene driven by a TRE sequence.

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v-erbA overexpression is required to extinguish c-erbA function in erythroid cell differentiation and regulation of the erbA target gene CAII.

Cited by 80 publications

References 53 publications

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

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

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

Molecular basis of the cell-specific activity of v-erb A in quail myoblasts

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