Interleukin-3, Erythropoietin, and Prolactin Activate a STAT5-like Factor in Lymphoid Cells

Pallard, Caroline; Gouilleux, Fabrice; Charon, M; Groner, Bernd; Gisselbrecht, Sylvie; Dusanter‐Fourt, Isabelle

doi:10.1074/jbc.270.27.15942

Cited by 120 publications

(78 citation statements)

References 31 publications

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“…To investigate if the Xmrk kinase is able to confer DNA binding activity to STAT5, BaF Hm cells were treated with EGF for 10 min and whole cell extracts were prepared. The extracts were incubated with magnetic beads coupled either to a multimerized oligonucleotide containing the STAT5 binding site derived from the b-casein promoter (wt-bCAS; Pallard et al, 1995) or to a multimerized mutated site with a destroyed STAT5 binding element (mu-bCAS). Bound proteins were eluted, separated by SDS ± PAGE and analysed by immunoblotting ®rst with anti-STAT5 and then with anti-phosphotyrosine ( Figure 5).…”

Section: Activation Of the Xmrk Kinase Induces Nuclear Translocation mentioning

confidence: 99%

“…After three freeze-thaw cycles lysates were centrifuged at 48C for 30 min at 10 000 g. The whole cleared supernatant was then incubated with 100 mg of M280-Streptavidin Dynabeads (Dynal) carrying either the STAT5 bCAS bindingsite (5'-GATCAGATTTCTAGGAATTCAATCC-3'; Pallard et al, 1995) derived from the bovine b-casein promoter or a mutated sequence (5'-GATCAGATT-TATTTTAATTCAATCC-3'), which does not possess the STAT5 binding motif 5'-TTCXXXGAA-3'. Double stranded oligonucleotides were end biotinylated and coupled to Dynabeads according to the manufacturer's instructions.…”

Section: Preparation Of Cell Extracts and Stat5 Dna-bindingmentioning

confidence: 99%

“…Both, EGF and PDGF mediated STAT5 tyrosine phosphorylation was detected in ®broblasts expressing the respective receptors (David et al, 1996;Vignais et al, 1996). However, apart from its activation through RTKs, STAT5 is playing its major role in signal transduction of the prolactin receptor and other cytokine receptors such as the IL-2-, IL-3-, the growth hormone and the erythropoietin (Epo) receptor in a variety of di erent cell types Ga en et al, 1995;Lin et al, 1996;Pallard et al, 1995;Xu et al, 1996). Some reports have attributed to STAT5 functions in cell proliferation (Mui et al, 1996), whereas in other cell systems STAT5 was described to participate in cell di erentiation (Mellitzer et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Signalling by the oncogenic receptor tyrosine kinase Xmrk leads to activation of STAT5 in Xiphophorus melanoma

et al. 1998

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Overexpression of the mutationally activated Xmrk receptor initiates the formation of hereditary malignant melanoma in the ®sh Xiphophorus. In addition to transcriptional overexpression a cell-type speci®c signal transduction is essential for Xmrk mediated tumor formation. To elucidate the consequence of Xmrk signalling and to identify target proteins that characterize the tumor phenotype, we analysed proteins that are strongly tyrosine phosphorylated in the ®sh melanoma cell line PSM. One of the most prominent phosphotyrosine proteins was found to be the signal transducer and activator of transcription STAT5. In a heterologous cell system (murine pro B-cells), activation of the Xmrk kinase in a chimeric receptor induced tyrosine phosphorylation, nuclear translocation and DNA binding of STAT5. Following receptor stimulation, expression of the STAT5 speci®c target genes cis, osm and pim-1 was induced. In Xiphophorus PSM cells STAT5 was found to be preferentially localized in the nucleus, but treatment with tyrphostin AG555, a speci®c Xmrk kinase-inhibitor, blocked nuclear localization. In these cells as well as in Xiphophorus melanoma expression of pim-1 and constitutive DNA-binding activity of STAT5 was detectable. This constitutive activity was higher in malignant than in benign melanomas, indicating that STAT5 activation is correlated with the malignancy of these tumors.

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Section: Activation Of the Xmrk Kinase Induces Nuclear Translocation mentioning

confidence: 99%

Section: Preparation Of Cell Extracts and Stat5 Dna-bindingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Signalling by the oncogenic receptor tyrosine kinase Xmrk leads to activation of STAT5 in Xiphophorus melanoma

et al. 1998

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“…To examine this point further, we infected progenitors with retrovirus encoding the wild-type PrlR. Like the EpoR, activation of the PrlR leads to Jak2 and STAT5 phosphorylation (35,42,43). In hematopoietic cell lines such as Ba/F3, transfected PrlR supports Prl-mediated cell proliferation (35,42) .…”

Section: Wild-type Prlr Can Fully Support Differentiation Of Erythroimentioning

confidence: 99%

The Prolactin Receptor and Severely Truncated Erythropoietin Receptors Support Differentiation of Erythroid Progenitors

Socolovsky

Dusanter‐Fourt

Lodish

1997

Journal of Biological Chemistry

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The EpoR 1 belongs to a large family of cytokine receptors, many of which are required for the proliferation and differentiation of hematopoietic as well as other cell types (4 -7). Throughout life, eight different hematopoietic lineages arise from pluripotent stem cells in the bone marrow (8, 9). The exact role of growth factors in this process is not clear and has been described broadly by two alternative hypotheses. The stochastic hypothesis suggests that commitment of a progenitor to a particular lineage is a stochastic event, subsequent to which cell differentiation proceeds along a predetermined program; growth factors are merely required to ensure the survival and proliferation of committed progenitors (10 -14). The contrasting inductive, or instructive, hypothesis attributes to growth factors a direct role in cell differentiation, predicting that growth factor receptors transduce signals that uniquely specify the differentiation outcome of a progenitor (15)(16)(17). A number of hybrid hypotheses have also been proposed, where, for example, committed progenitors arise stochastically, but their subsequent differentiation and acquisition of the mature phenotype are uniquely induced by lineage-specific growth factors (18).Although Epo is essential for the production of red blood cells, it is not thought to play a role in the generation of committed erythroid progenitors from pluripotent progenitors: expression of recombinant EpoR does not bias the lineage commitment of pluripotent hematopoietic progenitors (19,20), and normal numbers of committed erythroid BFU-e and CFU-e progenitors are found in the fetal livers of EpoR Ϫ/Ϫ mutant mice (21). However, there is a unique requirement for EpoR activation during the subsequent proliferation and terminal differentiation of committed erythroid progenitors: the EpoR Ϫ/Ϫ CFU-e and BFU-e progenitors fail to give rise to mature erythrocytes unless EpoR is expressed by retroviral infection (21); and in vitro, other growth factors only partially substitute for . It is not known whether EpoR activation is essential at this stage of erythroid differentiation because of an EpoR-unique instructive signal or whether it is simply required for functions that are not unique to EpoR, such as its proliferative and anti-apoptotic effects.Some evidence for the capability of EpoR to promote the erythroid phenotype comes from the ability of Epo to induce surface expression of glycophorin (25) and transcription of the ␤-globin gene (26, 27) in pre-B Ba/F3 cells expressing a transfected EpoR. However, the uncertain lineage commitment of many cell lines and their incomplete differentiation response makes them less suitable for the study of signaling in differentiation. EpoR-mediated signaling for proliferation can be studied in a number of interleukin-3-dependent cell lines, where heterologous expression of EpoR allows Epo to support cell proliferation (1, 2). Only the membrane proximal ϳ120 amino acids is essential for this function (1-3). Similarly truncated mutants of other cytokine r...

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“…This latter result favored an internal autocrine Epo stimulation of the cells. One of the intracellular events following binding of Epo to its surface receptors is the activation of the STAT5 transcription factor (Pallard et al, 1995;Wakao et al, 1995). Moreover, STAT5 activation seems to correlate with Epo-induced cellular proliferation (Damen et al, 1995;Gobert et al, 1996;.…”

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confidence: 99%

Abnormal erythropoietin (Epo) gene expression in the murine erythroleukemia IW32 cells results from a rearrangement between the G-protein β2 subunit gene and the Epo gene

et al. 1997

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Interleukin-3, Erythropoietin, and Prolactin Activate a STAT5-like Factor in Lymphoid Cells

Cited by 120 publications

References 31 publications

Signalling by the oncogenic receptor tyrosine kinase Xmrk leads to activation of STAT5 in Xiphophorus melanoma

Signalling by the oncogenic receptor tyrosine kinase Xmrk leads to activation of STAT5 in Xiphophorus melanoma

The Prolactin Receptor and Severely Truncated Erythropoietin Receptors Support Differentiation of Erythroid Progenitors

Abnormal erythropoietin (Epo) gene expression in the murine erythroleukemia IW32 cells results from a rearrangement between the G-protein β2 subunit gene and the Epo gene

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