PMID:17114416,9596579 As shown for DUSP6, binding to the substrate ERK2 MAPK then strongly increases the catalytic activity

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system PMID: 17114416,12444149 However, the role of ERK signaling in DUSP1 mRNA expression is not entirely clear, because the MEK-1 inhibitor U0126 was reported to block LPS-induced increases of DUSP1 at the mRNA and protein level PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process.

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system

PMID: 17114416,16184516,12193690 Mining of transcriptome datasets from primary mouse macrophages stimulated with LPS or the RAW 264.7 macrophage cell line after activation with a set of TLR ligands, our laboratory identified DUSP1, DUSP2, and DUSP16 as the most strongly induced MKP; thus, there is substantial overlap between these studies in the human and mouse system

PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process.

PMID: 17114416,12444149 However, the role of ERK signaling in DUSP1 mRNA expression is not entirely clear, because the MEK-1 inhibitor U0126 was reported to block LPS-induced increases of DUSP1 at the mRNA and protein level PMID: 17114416,10604989,10452980 Celada and colleagues then showed that DUSP1 is induced by signaling through the M-CSF receptor as well as in response to LPS, and additionally demonstrated the involvement of PKC in this process. PMID: 17114416,16184516,12356755,15590669,11742987 Consistent with a negative regulatory function for DUSP1 in macrophage activation, anti-inflammatory glucocorticoids increase DUSP1 expression in macrophages, and mast cells at the mRNA and protein level

PMID: 17114416,10570180,16375603 Serine phosphorylation of STAT1 mediated by p38 MAPK represents another example of cross-talk that may be indirectly controlled by DUSP proteins and contribute to the shaping of the transcriptional responses

PMID: 17114416,12459177,9804857 Curiously, there are reports from two different groups suggesting that DUSP1 dephosphorylates STAT1 at tyrosine residues in hepatocytes and vascular smooth muscle cells, which would imply a more direct interaction with the JAK-STAT pathway

PMID: 17114416 In contrast to DUSP6, the catalytic activity of DUSP10 is not increased by binding to p38 or JNK

PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS

PMID: 17114416,16461893 TLR stimuli increase DUSP1 expression through MyD88- or, in the case of poly(I:C), TRIF-dependent signaling

PMID: 17114416,16461893 TLR stimuli increase DUSP1 expression through MyD88- or, in the case of poly(I:C), TRIF-dependent signaling

PMID: 17114416,8557667 MAPK signaling controls DUSP1 expression at various levels. In fibroblasts, activation of the JNK pathway, but not of ERK, resulted in increased DUSP1 mRNA

PMID: 17114416,16184516,12356755,15590669,11742987 Consistent with a negative regulatory function for DUSP1 in macrophage activation, anti-inflammatory glucocorticoids increase DUSP1 expression in macrophages, and mast cells at the mRNA and protein level

PMID: 17114416,16184516 Recently, we found that the immunosuppressive cytokine IL-10 enhanced and prolonged DUSP1 expression in TLR-stimulated macrophages, acting in synergy with dexamethasone.

PMID: 17114416,16387640 Finally, the anti-inflammatory effects of the endocannabinoid anandamide on microglia have recently been correlated to up-regulation of DUSP1 protein levels, suggesting that signaling through the CB2 receptor is another pathway that leads to dampened MAPK activation through increased DUSP1 levels

PMID: 17114416,16387640 Finally, the anti-inflammatory effects of the endocannabinoid anandamide on microglia have recently been correlated to up-regulation of DUSP1 protein levels, suggesting that signaling through the CB2 receptor is another pathway that leads to dampened MAPK activation through increased DUSP1 levels

PMID: 17114416,12444149,15590669,15485842 A negative effect of DUSP1 on macrophage activation was suggested by overexpression of DUSP1, which was shown in a number of studies to inhibit phosphorylation of MAPK and the production of the cytokines TNF-{alpha} and IL-6 in response to diverse TLR stimuli

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PMID: 17114416 In contrast to DUSP6, the catalytic activity of DUSP10 is not increased by binding to p38 or JNK

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PMID: 17114416, 8626452 Cloned in 1993 as an immediate early gene from TCR-activated T cells, DUSP2/PAC-1 localizes to the nucleus and primarily inactivates p38 MAPK and ERK in vitro PMID: 17114416, 8626452 From overexpression studies in vitro, DUSP2 appeared to dephosphorylate p38 and ERK

PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data

PMID: 17114416,8649402 In another study, DUSP2 expression was found to be controlled by ERK activation

PMID: 17114416,8649402 In another study, DUSP2 expression was found to be controlled by ERK activation

PMID: 17114416, DUSP2 is induced in macrophages by TLR ligands and in mast cells by Fc{epsilon}RI ligation.

PMID: 17114416, DUSP2 is induced in macrophages by TLR ligands and in mast cells by Fc{epsilon}RI ligation.

PMID: 17114416, 8626452 Cloned in 1993 as an immediate early gene from TCR-activated T cells, DUSP2/PAC-1 localizes to the nucleus and primarily inactivates p38 MAPK and ERK in vitro PMID: 17114416, 8626452 From overexpression studies in vitro, DUSP2 appeared to dephosphorylate p38 and ERK

PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data

PMID: 17114416 Figure 1 PMID: 17114416 Finally, the authors also showed that DUSP2 physically interacts with p38, JNK, and ERK, providing a basis for the cross-talk between MAPK that is suggested by the data

PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.

PMID: 17114416,11971021,16713974,15107845 For example, IL-10 production was inhibited by the Map2k1/MEK1 inhibitor U0126, whereas IL-12 expression was suppressed by inhibition of p38 with SB203580

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,15067049,14607893 High levels of IL-10 along with low IL-12 production in response to TLR2 stimulation were shown to correlate with strong ERK activation, whereas TLR4, TLR5, or TLR9 ligands preferentially activated p38 and induced more IL-12

PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS

PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS

PMID: 17114416,15980098,12435740 Kovanen et al. analyzed T cell transcriptional responses to cytokine signaling through the common {gamma}-chain and identified DUSP5/VH3 and DUSP6/MKP-3 as up-regulated by IL-2, IL-7, and IL-15.

PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS

PMID: 17114416,11861597,7914033,9799232,9794373 All three MAPK are phosphorylated on the threonine and tyrosine residues of the shared TxY motif within minutes after TLR stimulation of macrophages and dendritic cells (DC) , as shown early on for the TLR4 ligand LPS