Activation of <i>junB</i> and <i>c‐myc</i> primary response genes by interleukin 9 in a human factor‐dependent cell line

Kang, Li Ya; Yang, Yu Chung

doi:10.1002/jcp.1041630324

Cited by 8 publications

(9 citation statements)

References 54 publications

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“…There is a growing amount of evidence that JunB may play a role distinct from that of c-Jun in the regulation of cell growth. junB expression is distinct from c-jun expression in many tissues (57) and during differentiation (25) and is stimulated independently of c-jun expression in response to a number of growth factors (1,37). c-Jun can homodimerize and heterodimerize with other AP1 factors, whereas JunB can only heterodimerize (20); furthermore, c-Jun strongly transforms rat embryo fibroblasts and transactivates via the TRE from a variety of promoters (58), whereas JunB is weakly transforming and its transactivation potential is more promoter specific (32).…”

Section: H Following Epo Stimulation Of Hcd57 Cells and Suppression mentioning

confidence: 99%

AP1 Regulation of Proliferation and Initiation of Apoptosis in Erythropoietin-Dependent Erythroid Cells

Jacobs-Helber

Wickrema

Birrer

et al. 1998

Molecular and Cellular Biology

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Section: H Following Epo Stimulation Of Hcd57 Cells and Suppression mentioning

confidence: 99%

AP1 Regulation of Proliferation and Initiation of Apoptosis in Erythropoietin-Dependent Erythroid Cells

Jacobs-Helber

Wickrema

Birrer

et al. 1998

Molecular and Cellular Biology

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“…hIL-9 has been demonstrated to induce c-Myc and JunB expression in a human megakaryocytic leukemia cell line (19). To understand the functional importance of the intracellular domains of hIL-9R␣ in the expression of primary response genes and to correlate expression of these genes with cell growth, we examined expression of c-myc, junB, c-jun, and c-fos in response to hIL-9 by Northern blot analysis.…”

Section: Il-9 Receptor ␣ Domains Critical For Signal Transductiondiffmentioning

confidence: 99%

“…Several homologous sequences, such as the BOX1 consensus sequence and a serine-rich region, which were demonstrated to be important for IL-2R␤ function (16), are also present in the cytoplasmic region of human IL-9R␣ (hIL-9R␣). Recently, it has been shown that several biochemical events including tyrosine phosphorylation of JAK kinases, activation of signal transducers and activators of transcription (STAT) proteins, and expression of nuclear protooncogenes are involved in IL-9-mediated signal transduction (17)(18)(19). In the present study, a series of deletions and point mutations were made in the cytoplasmic region of hIL-9R␣.…”

mentioning

confidence: 99%

Critical Cytoplasmic Domains of Human Interleukin-9 Receptor α Chain in Interleukin-9-mediated Cell Proliferation and Signal Transduction

Zhu¹,

Sun²,

Tsang³

et al. 1997

Journal of Biological Chemistry

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Interleukin-9 receptor (IL-9R) complex consists of a ligand-specific ␣ chain and IL-2R ␥ chain. In this study, two regions in the cytoplasmic domain of human IL-9R␣ were found to be important for IL-9-mediated cell growth. A membrane-proximal region that contains the BOX1 consensus sequence is required for IL-9-induced cell proliferation and tyrosine phosphorylation of Janus kinases (JAKs). Deletion of this region or internal deletion of the BOX1 motif abrogated IL-9-induced cell proliferation and signal transduction. However, substitution of the Pro-X-Pro in the BOX1 motif with Ala-X-Ala failed to abolish IL-9-induced cell proliferation but decreased IL-9-mediated tyrosine phosphorylation of JAK kinases, insulin receptor substrate-2, and signal transducer and activator of transcription 3 (STAT3) and expression of c-myc and junB. Another important region is downstream of the BOX1 motif and contains a STAT3 binding motif YLPQ. Deletion of this region significantly impaired IL-9-induced cell growth, activation of JAK kinases, insulin receptor substrate-2, and STAT3 and expression of early response genes. A point mutation changing YLPQ into YLPA greatly reduced IL-9-induced activation of STAT3 and expression of c-myc but did not affect cell proliferation. These results suggest that cooperation or cross-talk of signaling molecules associated with different domains of IL-9R␣ other than STAT3 is essential for IL-9-mediated cell growth. Interleukin 9 (IL-9)1 is a T cell-derived multifunctional growth factor that exerts its effects on activated T cells, B cells, mast cells, and hematopoietic progenitors (1, 2). The in vitro biological functions of IL-9 include its ability to stimulate proliferation of activated T cells, to enhance production of immunoglobulin in B cells, and to promote proliferation and differentiation of mast cells and hematopoietic progenitors (3-7). The involvement of IL-9 in lymphomagenesis has been suggested by in vivo studies (8) in which a higher susceptibility to T cell lymphoma was observed in transgenic mice expressing IL-9 constitutively and by in vitro experiments (9) in which IL-9 has been shown to protect mouse lymphoma cells from dexamethasone-induced apoptosis. The functions of IL-9 are mediated by the IL-9 receptor (IL-9R), which consists of a ligand-specific ␣ chain and IL-2 receptor (IL-2R) ␥ chain. IL-2R ␥ chain, normally referred to as the common ␥ chain (␥ c chain), is shared by receptors for IL-2, IL-4, IL-7, IL-9, and IL-15 (10 -13). Some of the signaling pathways elicited by these cytokines are quite similar, which probably explains in part the functional redundancy of these cytokines.IL-9R ␣ chain (IL-9R␣) is IL-9-specific and is responsible for IL-9 binding. The cDNAs encoding mouse and human IL-9R␣ have been cloned (14 -15). IL-9R␣ belongs to the hematopoietic receptor superfamily and has no intrinsic tyrosine kinase motif in its cytoplasmic region. Several homologous sequences, such as the BOX1 consensus sequence and a serine-rich region, which were demonstrated to be import...

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“…Our recent studies (9)(10)(11)(12) have shown that the induction of c-myc and junB, two primary response genes, is a signaling event downstream of JAK͞STAT (Janus kinase͞signal transducer and activator of transcription; refs. 13 and 14) activation in IL-9-mediated signal transduction.…”

mentioning

confidence: 99%

MRG1, the product of a melanocyte-specific gene related gene, is a cytokine-inducible transcription factor with transformation activity

Sun

Zhu

Yin

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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102

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Identification of cytokine-inducible genes is imperative for determining the mechanisms of cytokine action. A cytokine-inducible gene, mrg1 [melanocyte-specific gene (msg1) related gene], was identified through mRNA differential display of interleukin (IL) 9-stimulated and unstimulated mouse helper T cells. In addition to IL-9, mrg1 can be induced by other cytokines and biological stimuli, including IL-1␣, -2, -4, -6, and -11, granulocyte͞macrophage colonystimulating factor, interferon ␥, platelet-derived growth factor, insulin, serum, and lipopolysaccharide in diverse cell types. The induction of mrg1 by these stimuli appears to be transient, with induction kinetics similar to other primary response genes, implicating its role in diverse biological processes. Deletion or point mutations of either the Box1 motif (binds Janus kinase 1) or the signal transducer and activator of transcription 3 binding site-containing region within the intracellular domain of the IL-9 receptor ligand binding subunit abolished or greatly reduced mrg1 induction by IL-9, suggesting that the Janus kinase͞signal transducer and activator of transcription signaling pathway is required for mrg1 induction, at least in response to IL-9. Transfection of mrg1 cDNA into TS1, an IL-9-dependent mouse T cell line, converted these cells to IL-9-independent growth through a nonautocrine mechanism. Overexpression of mrg1 in Rat1 cells resulted in loss of cell contact inhibition, anchorageindependent growth in soft agar, and tumor formation in nude mice, demonstrating that mrg1 is a transforming gene. MRG1 is a transcriptional activator and may represent a founding member of an additional family of transcription factors.

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Activation of junB and c‐myc primary response genes by interleukin 9 in a human factor‐dependent cell line

Cited by 8 publications

References 54 publications

AP1 Regulation of Proliferation and Initiation of Apoptosis in Erythropoietin-Dependent Erythroid Cells

AP1 Regulation of Proliferation and Initiation of Apoptosis in Erythropoietin-Dependent Erythroid Cells

Critical Cytoplasmic Domains of Human Interleukin-9 Receptor α Chain in Interleukin-9-mediated Cell Proliferation and Signal Transduction

MRG1, the product of a melanocyte-specific gene related gene, is a cytokine-inducible transcription factor with transformation activity

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