scholarly journals Differential involvement of NF-κB and MAP kinase pathways in the generation of inflammatory cytokines by human neutrophils

2006 ◽  
Vol 81 (2) ◽  
pp. 567-577 ◽  
Author(s):  
Alexandre Cloutier ◽  
Thornin Ear ◽  
Emilie Blais-Charron ◽  
Claire M. Dubois ◽  
Patrick P. McDonald
Keyword(s):  
Map Kinase ◽  
Inflammatory Cytokines ◽  
Human Neutrophils ◽  
Differential Involvement ◽  
Map Kinase Pathways

scholarly journals Mitogen-Activated Protein (MAP) Kinase Pathways: Regulation and Physiological Functions*

2001 ◽  
Vol 22 (2) ◽  
pp. 153-183 ◽  
Author(s):  
Gray Pearson ◽  
Fred Robinson ◽  
Tara Beers Gibson ◽  
Bing-e Xu ◽  
Mahesh Karandikar ◽  
...  
Keyword(s):  
Map Kinase ◽  
Physiological Functions ◽  
Protein Map ◽  
Mitogen Activated Protein ◽  
Map Kinase Pathways

TOR and MAP kinase pathways synergistically regulate autophagy in response to nutrient depletion in fission yeast

Autophagy ◽  
2021 ◽  
pp. 1-16
Author(s):  
Cristina Corral-Ramos ◽  
Rubén Barrios ◽  
José Ayté ◽  
Elena Hidalgo
Keyword(s):  
Map Kinase ◽  
Fission Yeast ◽  
Nutrient Depletion ◽  
Map Kinase Pathways

Dual MAP kinase pathways mediate opposing forms of long-term plasticity at CA3–CA1 synapses

10.1038/80624 ◽  
2000 ◽  
Vol 3 (11) ◽  
pp. 1107-1112 ◽  
Author(s):  
V. Y. Bolshakov ◽  
L. Carboni ◽  
M.H. Cobb ◽  
S. A. Siegelbaum ◽  
F. Belardetti
Keyword(s):  
Map Kinase ◽  
Dual Map ◽  
Map Kinase Pathways

Inhibition of monocyte-derived inflammatory cytokines by IL-25 occurs via p38 Map kinase–dependent induction of Socs-3

Blood ◽  
2009 ◽  
Vol 113 (15) ◽  
pp. 3512-3519 ◽  
Author(s):  
Roberta Caruso ◽  
Carmine Stolfi ◽  
Massimiliano Sarra ◽  
Angelamaria Rizzo ◽  
Massimo C. Fantini ◽  
...  
Keyword(s):  
Map Kinase ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Human Peripheral Blood ◽  
Serum Levels ◽  
Cell Types ◽  
P38 Map Kinase ◽  
Negative Regulator ◽  
Therapeutic Implications

Abstract IL-25, a member of the IL-17 cytokine family, is known to enhance Th2-like responses associated with increased serum levels of IgE, IgG1, IgA, blood eosinophilia, and eosinophilic infiltrates in various tissues. However, IL-25 also abrogates inflammatory responses driven by Th17 cells. However, the cell types that respond to IL-25 and the mechanisms by which IL-25 differentially regulates immune reactions are not well explored. To identify potential targets of IL-25, we initially examined IL-25 receptor (IL-25R) in human peripheral blood cells. IL-25R was predominantly expressed by CD14+ cells. We next assessed the functional role of IL-25 in modulating the response of CD14+ cells to various inflammatory signals. CD14+ cells responded to IL-25 by down-regulating the synthesis of inflammatory cytokines induced by toll-like receptor (TLR) ligands and inflammatory cytokines. Inhibition of cytokine response by IL-25 occurred via a p38 Map kinase–driven Socs-3–dependent mechanism. In vivo, IL-25 inhibited monocyte-derived cytokines and protected against LPS-induced lethal endotoxemia in mice. These data indicate that IL-25 is a negative regulator of monocyte proinflammatory cytokine responses, which may have therapeutic implications.

ERK and p38 MAP kinase are involved in arachidonic acid release induced by H2O2 and PDGF in mesangial cells

2002 ◽  
Vol 282 (3) ◽  
pp. F485-F491 ◽  
Author(s):  
Misako Hayama ◽  
Risa Inoue ◽  
Satoshi Akiba ◽  
Takashi Sato
Keyword(s):  
Arachidonic Acid ◽  
Map Kinase ◽  
Mesangial Cells ◽  
P38 Map Kinase ◽  
Arachidonic Acid Release ◽  
Cytosolic Phospholipase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Acid Release ◽  
Map Kinase Pathways

Increased prostaglandin production is implicated in the pathogenesis of glomerular disease. With this consideration, we examined the combined effects of reactive oxygen species and platelet-derived growth factor (PDGF), which might initiate glomerular dysfunction, on arachidonic acid release and cytosolic phospholipase A2 (cPLA2) activation in rat mesangial cells. H2O2-induced release of arachidonic acid was enhanced by PDGF, which by itself had little effect on the release, and the enhancement was completely inhibited by a cPLA2 inhibitor. The phosphorylation of cPLA2, extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein (MAP) kinase was upregulated by H2O2 or PDGF alone and except for ERK was enhanced further by the two in combination. The release of arachidonic acid induced by PDGF together with H2O2 was inhibited partially by an inhibitor of ERK or p38 MAP kinase and completely when the two inhibitors were combined; the inhibitory pattern was similar to that for the phosphorylation of cPLA2. These results suggest that the ERK and p38 MAP kinase pathways are involved in the increase in cPLA2activation and arachidonic acid release induced by PDGF together with H2O2.

scholarly journals MAP kinase pathways

2005 ◽  
Vol 118 (16) ◽  
pp. 3569-3572 ◽  
Author(s):  
M. Qi
Keyword(s):  
Map Kinase ◽  
Map Kinase Pathways

scholarly journals Unfolded Protein Response Signaling and MAP Kinase Pathways Underlie Pathogenesis of Arsenic-Induced Cutaneous Inflammation

2011 ◽  
Vol 4 (12) ◽  
pp. 2101-2109 ◽  
Author(s):  
Changzhao Li ◽  
Jianmin Xu ◽  
Fugui Li ◽  
Sandeep C. Chaudhary ◽  
Zhiping Weng ◽  
...  
Keyword(s):  
Map Kinase ◽  
Unfolded Protein Response ◽  
Cutaneous Inflammation ◽  
Unfolded Protein ◽  
Protein Response ◽  
Map Kinase Pathways

scholarly journals Enhanced Survival of Wild-Type and Lurcher Purkinje Cells In Vitro Following Inhibition of Conventional PKCs or Stress-Activated MAP Kinase Pathways

2012 ◽  
Vol 12 (3) ◽  
pp. 377-389 ◽  
Author(s):  
Hadi S. Zanjani ◽  
Ann M. Lohof ◽  
Rebecca McFarland ◽  
Michael W. Vogel ◽  
Jean Mariani
Keyword(s):  
Map Kinase ◽  
Purkinje Cells ◽  
Wild Type ◽  
Map Kinase Pathways
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