Extracellular Signal-Regulated Kinase Induces the Megakaryocyte GPIIb/CD41 Gene through MafB/Kreisler

Sevinsky, Joel; Whalen, Anne M.; Ahn, Natalie G.

doi:10.1128/mcb.24.10.4534-4545.2004

Cited by 51 publications

(51 citation statements)

References 59 publications

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“…Maf family members also frequently cooperate with members of other transcription factor families (Ho et al, 1996,Huang et al, 2002,Rajaram and Kerppola, 2004,Sevinsky et al, 2004,Aramata et al, 2005 and can also interact with transcriptional coactivators, such as CREB-binding protein and p300 to activate gene transcription (Chen et al, 2002). In our hands co-transfection of c-Maf with either Ets-2 or c-Jun expression plasmids did not show synergistic effects between these transcription factors on the CD13 proximal promoter (data not shown).…”

Section: Discussionmentioning

confidence: 53%

CD13/APN transcription is regulated by the proto-oncogene c-Maf via an atypical response element

Mahoney

Petrović

Schacke

et al. 2007

Gene

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Angiogenic growth factors induce the transcription of the cell surface peptidase CD13/APN in activated endothelial cells of the tumor vasculature. Inhibition of CD13/APN abrogates endothelial invasion and morphogenesis in vitro and tumor growth in vivo suggesting a critical functional role for CD13 in angiogenesis. Experiments to identify the transcription factors responsible for this regulation demonstrated that exogenous expression of the proto-oncogene c-Maf, but not other bZip family members tested, potently activates transcription from a critical regulatory region of the CD13 proximal promoter between −115 and −70 bp which is highly conserved among mammalian species. Using promoter mutation, EMSA and ChIP analyses we established that both endogenous and recombinant c-Maf directly interact with an atypical Maf response element contained within this active promoter region via its basic DNA/leucine zipper domain. However full activity of c-Maf requires the amino-terminal transactivation domain, and site-directed mutation of putative phosphorylation sites within the transactivation domain (serines 15 and 70) shows that these sites behave in a dramatic cell type-specific manner. Therefore, this atypical response element predicts a broader range of c-Maf target genes than previously appreciated and thus impacts its regulation of multiple myeloma as well as endothelial cell function and angiogenesis.

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Section: Discussionmentioning

confidence: 53%

CD13/APN transcription is regulated by the proto-oncogene c-Maf via an atypical response element

Mahoney

Petrović

Schacke

et al. 2007

Gene

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“…GPIIb combines with the more broadly expressed b3 (GPIIIa, CD61) subunit to form the GPIIb/IIIa heterodimer receptor that regulates cell adhesion and functions in aggregation of activated platelets by binding fibrinogen and vWF (Jackers et al, 2004;Sevinsky et al, 2004). Because of its unique expression in megakaryocytes and platelets in humans, in this study GPIIb was chosen as a model for IL-13-dependent regulation of lineage-specific marker.…”

Section: Discussionmentioning

confidence: 99%

IL‐13 upregulates GPIIb expression in megakaryocytic cell lines via STAT6

Shi

Cai

Zhou

et al. 2010

The Anatomical Record

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Interleukin 13 (IL-13) is a key cytokine involved in the regulation of inflammatory, immune responses, and cell differentiation. The present study was to investigate the effect of IL-13 on the expression of glycoprotein IIb (GPIIb), a megakaryocytic gene, in Dami cells (human megakaryoblastic leukemia cell line) and HEL cells (human erythroleukemic cell line, which has both erythroid and megakaryocytic markers). Furthermore, it addresses the mechanisms governing the regulation of GPIIb expression by IL-13. The molecular responses of Dami cells and HEL cells to IL-13 treatment were analyzed by RT-PCR, Western blot, chromatin immunoprecipitation (ChIP) and flow cytometry analysis. We show that IL-13Ra1 and IL-4Ra are expressed in Dami cells and HEL cells. The expression of GPIIb was significantly upregulated at the mRNA and protein levels by treatment with IL-13. Moreover, IL-13 induced phosphorylation of signal transducer and activator of transcription 6(STAT6). By using a STAT6-specific antibody and PCR primers designed to yield a product, which encompasses the STAT6 binding site of the GPIIb promoter, we have shown the binding of the IL-13-mediated activation of STAT6 to the promoter of GPIIb gene. These results broaden the involvement of IL-13 into megakaryocyte differentiation by STAT6 pathway.

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“…MAF-B is a bZIP transcription factor belonging to the large MAF sub-class, which is able to act either as a repressor or an activator depending on its interacting partners in various differentiation processes. MAF-B interaction with ets transcription factor appears to be required for the down-regulation of erythroid genes such as ß-globin (28) and the up-regulation of the CD41 marker during the megakaryocytic differentiation (27). Moreover, MAF-B is crucial for the differentiation of non-adherent macrophages and expression of the macrophage marker F4/80 (41) as well as for the control of the balance between dendritic and monocytic differentiation (25,26,42).…”

Section: Discussionmentioning

confidence: 99%

“…2). The expression of the transcription factor MAF-B was followed since its expression was associated with monocyte/macrophage (25,26) and megakaryocytic differentiation (27,28).…”

Section: All Three Wnt13 Mrna Isoforms Are Expressed In Human Cellsmentioning

confidence: 99%

Differential expression of Wnt13 isoforms during leukemic cell differentiation

Bunaciu

Tang²,

Mao³

2008

Oncol Rep

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Abstract. Wnt proteins control cell fate and differentiation during development. Alterations of the Wnt/ß-catenin signaling pathway and changes in wnt gene expression are clearly associated with leukemia. The expression of human wnt13/ wnt2b is complex as it involves alternative promoters and RNA splicing giving rise to Wnt13A, -B and -C mRNA isoforms, which encode proteins with different intracellular localizations and functions. We investigated the expression of the human wnt13 in relation to leukemic cell differentiation. Differentiated endothelial cells expressed the highest levels of Wnt13 mRNA isoforms among various endothelial and leukemic cell lines. The differentiation of U937 cells towards monocyte/macrophages resulted in an increase of Wnt13B and -C mRNAs while Wnt13A mRNAs were decreased. The differentiation of K562 cells towards megakaryocytes was accompanied with the up-regulation of all Wnt13 mRNA isoforms. In the two differentiation systems, Wnt13B and -C expression correlated with the expression of the MAF-B transcription factor. Our data demonstrate the differential regulation of wnt13 promoters and pinpoint a Wnt13 isoform switch during differentiation of the leukemic U937 cells towards the monocyte/macrophage lineage, thereby suggesting new players in this process.

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Extracellular Signal-Regulated Kinase Induces the Megakaryocyte GPIIb/CD41 Gene through MafB/Kreisler

Cited by 51 publications

References 59 publications

CD13/APN transcription is regulated by the proto-oncogene c-Maf via an atypical response element

CD13/APN transcription is regulated by the proto-oncogene c-Maf via an atypical response element

IL‐13 upregulates GPIIb expression in megakaryocytic cell lines via STAT6

Differential expression of Wnt13 isoforms during leukemic cell differentiation

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