Parallel signal processing among mammalian MAPKs

Cano, Eva; Mahadevan, Louis C.

doi:10.1016/s0968-0004(00)88978-1

Cited by 965 publications

(696 citation statements)

References 42 publications

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“…53,54 MAPKs are intracellular serine/threonine kinases 55 and the three most intensively studied kinases are the ERK, c-jun NH2-terminal kinase, and p38. 53,56,57 Kit, proteinkinase B (PKB)/Akt and MAPK are expressed in a high percentage of small cell lung cancers. 55 Furthermore, miRNAs targeting the PI3K/ Akt/mTOR signaling pathway were differentially expressed in the four types of pulmonary neuroendocrine tumors investigated in this study.…”

Section: Discussionmentioning

confidence: 99%

Different micro-RNA expression profiles distinguish subtypes of neuroendocrine tumors of the lung: results of a profiling study

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Different micro-RNA expression profiles distinguish subtypes of neuroendocrine tumors of the lung: results of a profiling study

et al. 2014

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“…To determine whether Hog1 is phosphorylated upon treatment with l-dopa, we performed Western blot analysis by using phospho-p38 antibody. The antibody recognizes the TGY motif characteristic of stress-activated mitogen-activated protein kinases activated by phosphorylation of threonine and tyrosine (Cano and Mahadevan, 1995). It has been used for detecting activated Hog1 (Maeda et al, 1994).…”

Section: Kss1 and Mpk1 Are Phosphorylated Upon Treatment With L-dopamentioning

confidence: 99%

Oxidative Stress ActivatesFUS1andRLM1Transcription in the YeastSaccharomyces cerevisiaein an Oxidant-dependent Manner

Staleva

Hall

Orlow

2004

MBoC

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Mating in haploid Saccharomyces cerevisiae occurs after activation of the pheromone response pathway. Biochemical components of this pathway are involved in other yeast signal transduction networks. To understand more about the coordination between signaling pathways, we used a "chemical genetic" approach, searching for compounds that would activate the pheromone-responsive gene FUS1 and RLM1, a reporter for the cell integrity pathway. We found that catecholamines (L-3,4-hydroxyphenylalanine [L-dopa], dopamine, adrenaline, and noradrenaline) elevate FUS1 and RLM1 transcription. N-Acetyl-cysteine, a powerful antioxidant in yeast, completely reversed this effect, suggesting that FUS1 and RLM1 activation in response to catecholamines is a result of oxidative stress. The oxidant hydrogen peroxide also was found to activate transcription of an RLM1 reporter. Further genetic analysis combined with immunoblotting revealed that Kss1, one of the mating mitogen-activated protein kinases (MAPKs), and Mpk1, an MAPK of the cell integrity pathway, participated in L-dopa-induced stimulation of FUS1 and RLM1 transcription. We also report that Mpk1 and Hog1, the high osmolarity MAPK, were phosphorylated upon induction by hydrogen peroxide. Together, our results demonstrate that cells respond to oxidative stress via different signal transduction machinery dependent upon the nature of the oxidant. INTRODUCTIONIn the haploid cells of the yeast Saccharomyces cerevisiae, four essential MAPK cascades (Figure 1) respond to different external signals to mediate specific responses. The mating pathway is activated by peptide pheromones and induces cell-cycle arrest and the morphological changes required for mating (Elion, 1998;Gustin et al., 1998). The invasive growth pathway is activated by starvation and induces foraging into the agar substratum. The high osmolarity glycerol (HOG) pathway increases intracellular glycerol levels in response to hypertonic stress, whereas the cell integrity pathway is activated by hypotonic stress, heat shock, or impaired cell wall synthesis. Recently, an additional MAPK cascade has been described: the Kss1 vegetative growth pathway (Lee and Elion, 1999). The Kss1 pathway may be activated by cell wall stress or changes in osmolarity (Cullen et al., 2000).The mating pathway is the most studied cellular response to an external signal. As a relatively simple G protein-coupled cascade, it is a widely used model to study mammalian G protein-coupled receptors. The mating cascade includes pheromone receptors (Ste2 and Ste3), G proteins (Gpa1, Ste4, and Ste18), the p21 activating protein kinase Ste20, a mitogen-activated protein kinase kinase kinase (MAPKKK) Ste11, a mitogen-activated protein kinase kinase (MAPKK) Ste7, a scaffolding protein Ste5 and two MAPKs (Fus3 and Kss1) (Gustin et al., 1998;Madhani and Fink, 1998;Farley et al., 1999). Targets of the terminal MAPK include Ste12, a factor required for transcription of pheromone-responsive genes, and Far1, a bifunctional protein required for polarization and G1...

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“…For example, IL-1 can induce proliferation of rat mesangial cells [3], but not of human cells [4]. Intracellular protein kinases like the mitogen-activated protein kinases (MAPKs) are key molecules transducing extracellular signals into the nucleus [5]. Depending on the tissue or cell system studied IL-*Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

et al. 1996

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Interleukin 1 (IL-I) potently activates human glomerular mesangial cells (HMC).In cytosolic extracts of IL-1-stimulated HMC or in anion exchange chromatography fractions we could not find any change in phosphorylation of myelin basic protein (MBP), a good substrate for extracellular regulated kinase (ERK). In contrast, IL-I stimulated GST-jun kinase activity at least 10-fold. The jun kinase activity could be charaeterised as JNK1 and JNK2 at the protein and mRNA level. IL-I, TNF, UV light and osmotic stress, but not PMA, LPS, IL-3, IL-4, IL-6, IL-8, IL-10, IL-13, GM-CSF, PDGF, bFGF, TGF-[~ and interferon-T were able to stimulate jun kinase activity in HMC, suggesting that jun kinase is selectively mediating signal transduction of the proinflammatory cytokines IL-1 and TNF as well as of cellular stress in HMC.

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Parallel signal processing among mammalian MAPKs

Cited by 965 publications

References 42 publications

Different micro-RNA expression profiles distinguish subtypes of neuroendocrine tumors of the lung: results of a profiling study

Different micro-RNA expression profiles distinguish subtypes of neuroendocrine tumors of the lung: results of a profiling study

Oxidative Stress ActivatesFUS1andRLM1Transcription in the YeastSaccharomyces cerevisiaein an Oxidant-dependent Manner

Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

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