Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase.

Bruder, Joseph T.; Heidecker, Gisela; Rapp, Ulf R.

doi:10.1101/gad.6.4.545

Cited by 446 publications

(379 citation statements)

References 49 publications

(56 reference statements)

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“…To further con®rm the involvement of these pathways, we carried out Elk-1 transactivation studies with dominant negative constructs of Raf-1 and the p85 subunit of PI3 kinase (Bruder et al, 1992;Brennan et al, 1997). These constructs did not only abrogate the DHT e ect but they also reduced the basal activity which possibly arose as a result of residual hormone in the culture medium (Figure 5a).…”

Section: Sensitivity To Kinase Inhibitorsmentioning

confidence: 99%

“…Kinase inhibitors PD98059, GF109203X, and Wortmannin were all purchased from Calbiochem (Bad Soden/Taunus, Germany). The indicator gene consisting of GAL 4 DNA binding sites controlling the expression of a luciferase gene pG5.E4D38lux3, the expression vector containing the GAL 4 DNA binding domain (DBD) alone or linked to the transcription factor Elk-1, the empty expression vector containing the RSV promoter RSV-H20 and the RSV promoter driving the expression of a dominant negative Raf-1 sequence RSV-cRafC4 have all been described (O ringa et al, 1990;Bruder et al, 1992;Gille et al, 1995b;Kamano et al, 1995).…”

Section: Materials and Plasmid Constructsmentioning

confidence: 99%

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Rapid signalling by androgen receptor in prostate cancer cells

Peterziel¹,

Mink²,

Schonert³

et al. 1999

Oncogene

234

157

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Androgens are important growth regulators in prostate cancer. Their known mode of action in target cells requires binding to a cytoplasmic androgen receptor followed by a nuclear translocation event and modulation of the expression of speci®c genes. Here, we report another mode of action of this receptor. Treatment of androgen responsive prostate cancer cells with dihydrotestosterone leads to a rapid and reversible activation of mitogen-activated protein kinases MAPKs (also called extracellular signal-regulated kinases or Erks). Transient transfection assays demonstrated that the androgen receptor-mediated activation of MAP kinase results in enhanced activity of the transcription factor Elk-1. This action of the androgen receptor di ers from its known transcriptional activity since it is rapid and insensitive to androgen antagonists such as hydroxy¯utamide or casodex. Biochemical studies as well as analyses with dominant negative mutants showed the involvement of kinases such as MAPK/Erk kinase, phosphatidyl-inositol 3-kinase and protein kinase C in the androgen receptormediated activation of MAP kinase. These results demonstrate a novel regulatory action of the androgen receptor and prove that in addition to its known transcriptional e ects, it also uses non-conventional means to modulate several cellular signalling processes.

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Section: Sensitivity To Kinase Inhibitorsmentioning

confidence: 99%

Section: Materials and Plasmid Constructsmentioning

confidence: 99%

Rapid signalling by androgen receptor in prostate cancer cells

Peterziel¹,

Mink²,

Schonert³

et al. 1999

Oncogene

234

157

View full text Add to dashboard Cite

show abstract

“…The ERK1 and ERK2 constructs contain the coding region of these MAPKs in which the conserved lysine involved in phosphate transfer (codon 71 and 52 for ERK1 and ERK2 respectively) has been changed to arginine thus impairing the catalytic e ciency (Frost et al, 1994). The Raf C4 expression plasmid encodes the c-Raf-1 protein lacking the kinase domain (Bruder et al, 1992). The MEK DN3S218E-S222D construct encodes the MEK1 sequence in which residues 32 ± 51 at the aminoterminus have been deleted and in which the serines at position 218 and 222 have been replaced by glutamate and aspartate respectively (Mansour et al, 1994).…”

Section: Vectors and Antibodiesmentioning

confidence: 99%

Elevated urokinase-type plasminogen activator receptor expression in a colon cancer cell line is due to a constitutively activated extracellular signal-regulated kinase-1-dependent signaling cascade

et al. 1997

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“…Our results indicate that the activation of c-jun is a consequence of JNK-1 and c-Raf-1 activation. c-Raf-1 may exert nuclear events directly after translocating to the nucleus where it enhances the expression of several genes, including c-jun, through Ets-1 and AP-1-binding sites [55][56][57]. Also, c-Raf-1 phosphorylates c-jun [58].…”

mentioning

confidence: 99%

CREB and AP‐1 activation regulates MKP‐1 induction by LPS or M‐CSF and their kinetics correlate with macrophage activation versus proliferation

et al. 2009

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MAPK phosphatase-1 (MKP-1) is a protein phosphatase that plays a crucial role in innate immunity. This phosphatase inactivates ERK1/2, which are involved in two opposite functional activities of the macrophage, namely proliferation and activation. Here we found that although macrophage proliferation and activation induce MKP-1 with different kinetics, gene expression is mediated by the proximal promoter sequences localized between À380 and À180 bp. Mutagenesis experiments of the proximal element determined that CRE/AP-1 is required for LPS-or M-CSF-induced activation of the MKP-1 gene. Moreover, the results from gel shift analysis and chromatin immunoprecipitation indicated that c-Jun and CREB bind to the CRE/AP-1 box. The distinct kinetics shown by M-CSF and LPS correlates with the induction of JNK and c-jun, as well as the requirement for Raf-1. The signal transduction pathways that activate the induction of MKP-1 correlate kinetically with induction by M-CSF and LPS.Key words: Activation . Kinases . Macrophage . Phosphatases . Proliferation IntroductionMacrophages perform critical functions during the immune response. These cells are regulators of homeostasis and play an important role in innate and acquired immunity during infection, tumor growth, and wound healing [1]. In response to needs, tissue macrophages proliferate, further differentiate to more specialized macrophagic populations, or become activated. Macrophages, like many other cells of the immune system, are produced in large excess and most undergo apoptosis [2].In the presence of M-CSF, macrophages differentiate and proliferate. However, the proliferation of these cells is blocked when they are activated by Gram-negative LPS or by . Activation causes many biochemical, morphological and functional modifications. Macrophage response to M-CSF and LPS involves the phosphorylation of the three members of the MAPK family [4].MAPK are critical components of signal transduction pathways activated by a range of stimuli and they mediate a number of physiological and pathological changes in cell function [5,6]. MAPK activation requires phosphorylation on a threonine and tyrosine residue located in the activation loop. This process is reversible even in the continued presence of activating stimuli, thereby indicating that protein phosphatases regulate MAPK [7]. Although MAPK are conserved evolutionary pathways present in eukaryotic cells, the kinetics of activation and their subcellular compartmentalization are cell type-specific, and they orchestrate differential cellular responses. For example, in neuronal cells, sustained MAPK phosphorylation of even days is required for cellular activation or differentiation, while in fibroblasts, phosphorylation of this kinase family is very short. In contrast, to Immunol. 2009. 39: 1902-1913 Cristina Casals-Casas et al. 1902 achieve proliferation, extended activation of MAPK is required in these cells [6,7]. The correct spatio-temporal regulation of MAPK signalling is crucial in determining cellular responses to g...

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Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase.

Cited by 446 publications

References 49 publications

Rapid signalling by androgen receptor in prostate cancer cells

Rapid signalling by androgen receptor in prostate cancer cells

Elevated urokinase-type plasminogen activator receptor expression in a colon cancer cell line is due to a constitutively activated extracellular signal-regulated kinase-1-dependent signaling cascade

CREB and AP‐1 activation regulates MKP‐1 induction by LPS or M‐CSF and their kinetics correlate with macrophage activation versus proliferation

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