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PMID |
Sentence |
1 |
12686724
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Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2.
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2 |
12686724
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Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression.
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3 |
15893422
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We also investigated whether specific inhibition of p38 and Erk1/2 MAPK would inhibit TNF-alpha and IL-6 production and thus astrocyte apoptosis, and proliferation, respectively.
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4 |
16641451
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Herein, we show that SAG induces extracellular signal-regulated kinase 1 (ERK-1) and ERK-2 phosphorylation through phosphoinositide 3-kinase (PI3K), protein kinase C, and Ras activation and p38 mitogen-activated protein kinase (MAPK) phosphorylation through PI3K and Akt activation.
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5 |
16641451
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ERK-1 and ERK-2 activation results in an increase in the production of reactive oxygen species (ROS) 3 to 6 h after SAG treatment, while p38 MAPK activation and subsequent tumor necrosis factor alpha release result in the production of nitric oxide (NO) 24 h after SAG treatment.
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6 |
16893987
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Activation of GA-12 (a repressor element of IL-12 p40), rather than suppression of promoter elements, such as binding sites for NF-kappaB, AP-1, and IRF-1, was detected in LPS-stimulated RAW264.7 cells, accompanying hyperactivation of extracellular signal-related kinase (ERK).
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7 |
16826166
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We report that in the presence of urokinase plasminogen activator (uPA), overexpression of GM3 paradoxically increases the proliferation of carcinoma cells by augmenting ERK-independent p70S6 kinase activation.
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8 |
16826166
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The ERK-independent activation of p70S6 kinase involves phosphorylation at threonine-389, threonine-421/serine-424, and serine-411 sites with intermediate phosphatidylinositol 3 kinase and protein kinase C-zeta activation.
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9 |
18180378
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Activation of extracellular signal-regulated kinase (ERK) increased TGF-beta expression while expression of a constitutively activated interferon regulatory factor-3 (IRF3) stimulated IL-10 secretion by DCs.
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10 |
18322186
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We found that TLR ligands also promote the induction of IL-10-secreting regulatory T (Treg) cells through p38 MAPK-induced IL-10 production by dendritic cells (DC).
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11 |
18322186
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Inhibition of p38 suppressed TLR-induced IL-10 and PGE(2) and enhanced IL-12 production in DC.
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12 |
18322186
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In addition, inhibition of p38 enhanced the antitumor therapeutic efficacy of DC pulsed with Ag and CpG and this was associated with an enhanced frequency of IFN-gamma-secreting T cells and a reduction of Foxp3(+) Treg cells infiltrating the tumors.
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13 |
18579695
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Thus, these results indicate that the MEK1/2 and p38 MAPK signaling pathways play a critical role in the regulation of inducible LL-37 gene expression in A549 cells infected with M. bovis BCG.
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14 |
18708593
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DnaK induced the activation of MAPKs and NF-kappaB in DC and the production of the proinflammatory cytokines IL-6, TNF-alpha, and IL-12 p40, as well as low levels of IL-10.
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15 |
18708593
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DnaK induced activation of MAPKs and NF-kappaB in a MyD88- or TRIF-dependent manner.
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16 |
18809662
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Since the V. cholerae genome encodes five distinct flagellin proteins, FlaA to FlaE, with homology to conserved TLR5 recognition regions of Salmonella FliC, we hypothesized that V. cholerae flagellins may contribute to IL-8 induction through TLR5 and mitogen-activated protein kinase (MAPK) signaling.
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17 |
19828771
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A specific p38 MAPK inhibitor strongly inhibited V. parvula LPS-induced TNF-alpha, IL-1beta, IL-6, and IL-10.
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18 |
19828771
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V. parvula LPS-stimulated cytokine induction, as well as p38 MAPK activation, are TLR4-dependent features.
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19 |
20702733
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Inhibition of Smad-signaling and p38 MAPK-signaling indicated that apoptosis of IH-1 cells is dependent on Smad-signaling downstream of BMP, whereas the antiproliferative effect of BMP-2 on IH-1 cells also involves p38 MAPK-signaling.
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20 |
20725863
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The P38 and ERK Mitogen-Activated Protein Kinase (MAPK) pathways govern the regulation of cytokines (IL-2, IL-10, and TNF-?) as well biomarkers (PD-1, Fas/FasL, among others) that are skewed in chronic HIV infection.
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21 |
20725863
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HIV utilizes the P38 and ERK pathways to produce new virions and to deplete CD4+ T cells from the host's immune system.
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22 |
21098227
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The enhanced cytokine expression was accompanied by enhanced activation of p38 MAPK and ERK1/2, both of which were critical for LVS-induced expression of TNF and IL-6.
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23 |
21098227
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LVS-induced MAPK activation and cytokine production were TLR2- and MyD88- dependent.
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24 |
21098227
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Peak levels of MKP-1 correlated closely with the decline in p38 MAPK and ERK1/2 phosphorylation.
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25 |
21098227
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These data suggest that infection by LVS restrains the TLR2-triggered proinflammatory response via parallel activation of PI3K, leading to enhanced MKP-1 expression, accelerated deactivation of MAPKs, and suppression of proinflammatory cytokine production.
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26 |
21134826
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First, HBV DNA can be recognized by DCs through toll-like receptor 9 (TLR9) which activates the NF-?B signal pathway and p38 MAPK to up-regulate the expression of interferon (IFN) regulatory factor 7 (IRF-7) in a manner independent of type I IFN signaling, resulting in secretion of type I IFN and inflammatory cytokines, and induction of DC maturation and the adaptive immune response.
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27 |
21199725
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Here we assess the role of reactive oxygen species (ROS) in the secretion of the CCL2 and the activation of mitogen-activated protein kinases (MAPKs) by human monocytic cells infected with Mycobacterium bovis bacillus Calmette Guérin (BCG).
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28 |
21199725
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Analysis of downstream signals showed that inhibition of NADPH oxidase inhibited M. bovis BCG-induced phosphorylation of MAPK (extracellular signal-regulated kinase (ERK) 1/2 and p38).
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29 |
21199725
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These results strongly suggest that NADPH oxidase-derived ROS-mediated activation of p38 and ERK 1/2 is essential for the M. bovis BCG-induced CCL2 production.
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30 |
21271951
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We also discuss pharmacological approaches to modulation of MAP kinase signaling for manipulation of the functional plasticity of DC, such that they may be directed to promote T(H)17 responses following DC vaccination.
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31 |
21490151
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LT enhanced IL-23 and IL-1? production from DCs via activation of ERK MAPK and IL-1? secretion through activation of caspase-1 and the NLRP3 inflammasome.
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32 |
21450974
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The objectives of this study were to examine the roles of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-?B [NF-?B] and activating protein 1 [AP-1]) in peptidoglycan (PGN)-induced iNOS expression and NO production in macrophages.
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33 |
21450974
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PGN stimulates the activation of all three classes of MAPKs, extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and p38(mapk) in macrophages, albeit with differential activation kinetics.
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34 |
21450974
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In contrast, inhibition of the ERK pathway using PD98059 dose dependently enhanced PGN-induced iNOS expression and NO production.
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35 |
21450974
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An electrophoretic mobility shift assay showed that SP600125 inhibited PGN-induced NF-?B and AP-1 activation, whereas inhibition of the ERK pathway enhanced NF-?B activation, but with no effect on AP-1.
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36 |
21450974
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These results indicate that the JNK MAPK positively regulate PGN-induced iNOS and NO expression by activating NF-?B and AP-1 transcription factors, whereas the ERK pathway plays a negative regulatory role via affecting NF-?B activity.
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37 |
21600652
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Collectively, we suggest that S. aureus-induced IL-1? production requires lipid raft formation, activation of MAP kinases, and activation of transcription factors AP-1, CRE, and NF-?B.
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38 |
19540594
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Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta.
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39 |
21901556
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E. coli activates TLR4, which is responsible for the activation of IL-12, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).
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