INT110021
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Mouse preimplantation embryo responses to culture medium osmolarity include increased expression of CCM2 and p38 MAPK activation
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Upon SOD2 overexpression, the deficits in axonal transport recovered in association with restoration of levels of phosphorylated p38 MAPK and tau protein. | |||||||||||||||
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TA muscles transfected with empty vector, dominant negative forms of p38? | |||||||||||||||
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A unique feature of our studies is the comparison of stimulation-induced global gene expression between p38? | |||||||||||||||
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In addition, in a model of anoxia-reoxygenation-induced lung endothelial cell apoptosis, SB203580 or transfection with a p38? | |||||||||||||||
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In addition, in a model of anoxia-reoxygenation-induced lung endothelial cell apoptosis, SB203580 or transfection with a p38? | |||||||||||||||
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In addition, protein kinase C (PKC) inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) and chelerythrine, significantly inhibited guanfacine-induced interleukin-12 production and p38 MAPK in a concentration-dependent manner. | |||||||||||||||
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Our finding that muscle-specific overexpression of a dominant negative form of p38? | |||||||||||||||
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For example, gene expression of MAPK8 and MAPK14, both of which are involved in the MAPK pathway, was upregulated (13.15-fold and 4.17-fold, resp.) in the berberine group. | |||||||||||||||
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RT2 profiler PCR array analysis showed that berberine
upregulated the expression of glucose transporter 4 (GLUT4), mitogen-activated protein kinase 14 (MAPK14), MAPK8(c-jun N-terminal kinase, JNK), peroxisome proliferator-activated receptor ? | |||||||||||||||
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mRNA following motor nerve stimulation; however, TA muscles transfected with the dominant negative p38? | |||||||||||||||
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MKO mice and in skeletal muscle transfected with dominant negative p38? | |||||||||||||||
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mRNA following motor nerve stimulation; however, TA muscles transfected with the dominant negative p38? | |||||||||||||||
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There was a non-significant trend towards increased levels of CB1/CB2 receptor expression in diabetic spinal cord specimens over time, while p-p38 MAPK expression elevated during the course of diabetes until the final time point when it declined (Figure 3). | |||||||||||||||
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MCAO followed by 6 hour reperfusion caused increased levels of phosphorylated p38 MAPK that were significantly higher in the ischemic hemisphere of the cPLA2? | |||||||||||||||
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Lignocaine and TTX significantly attenuated the effects of LPS on TLR-4, NF-kappaB, ERK and p38 MAPK expression, but not on JNK. | |||||||||||||||
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We treated microglial cells with SB203580 (SB, 5 µM; an inhibitor of p38 MAPK) or PD98059 (PD, 5 µM; a selective inhibitor of p44/42) for 1 h prior to treatment with LPS (100 ng/mL) for 30 minutes, and found both inhibitors markedly suppressed the activation of LPS-induced p38 or p44/42 MAPKs (Fig. 2A, B). | |||||||||||||||
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The expression of p38 mitogen-activated protein kinase (MAPK) is elevated in the peripheral lungs and alveolar macrophages in patients with mild or moderate COPD compared with smokers.90 This study also suggested an inverse correlation between the activation of p38 MAPK and the reduction in FEV1 and FEV1/FVC.90 An elevation of p38 MAPK may be responsible for an increase in phosphorylation of GR? | |||||||||||||||
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p38-mediated mitochondrial-dependent caspase-3 activation and apoptosis | |||||||||||||||
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Inflammatory stimuli activate the three MAPK major pathways: extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK pathways. | |||||||||||||||
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General Comments
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