INT75497
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
After 1 h or 96 h of treatment, Fos and Jun protein levels were altered and the DNA-binding activity of AP-1 was increased in response to both substances. | |||||||||||||||
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This effect was specific, as the activity of nuclear factor kappabeta, nuclear factor of activated T cells, and specific protein-1 was not altered and several other volatile anesthetics studied did not affect AP-1 activation. | |||||||||||||||
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Neurotoxicity of lidocaine involves specific activation of the p38 mitogen-activated protein kinase, but not extracellular signal-regulated or c-jun N-terminal kinases, and is mediated by arachidonic acid metabolites. | |||||||||||||||
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Osmotic and glutamate receptor regulation of c-Jun NH(2)-terminal protein kinase in neuroendocrine cells. | |||||||||||||||
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We report that in human colorectal carcinoma cells NSAIDs stimulated the three families of MAPK, extracellular regulated kinases, c-Jun N-terminal kinases, p38 MAPK and that this stimulation is prevented by N-acetyl cysteine. | |||||||||||||||
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Furthermore, c-Jun immunoreactivity was also observed in disc cell clusters, thus demonstrating them to be active transcriptional sites in disc tissue. c-Fos immunoreactivity was seen in 15/38 and c-Jun in 28/38 herniated discs (39% and 74% respectively). | |||||||||||||||
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In order to approach the astroglial implication of addictive and neurotoxic processes associated with psychostimulant drug abuse, the effects of amphetamine or cocaine (1-100 microM) on redox status, AP-1 transcription factor and pro-enkephalin, an AP-1 target gene, were investigated in the human astrocyte-like U373 MG cells. | |||||||||||||||
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Because astrocytes interact extensively with the neurons in the brain, our data led us to conclude that oxidation-regulated AP-1 target genes may represent one of the molecular mechanisms underlying neuronal adaptation associated with psychostimulant dependence. | |||||||||||||||
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BACKGROUND: To explore whether cytotoxicity of local anesthetics is related to apoptosis, the authors examined how local anesthetics affect mitogen-activated protein kinase (MAPK) family members, extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinases (JNKs)-stress-activated protein kinases, and p38 kinase, which are known to play important roles in apoptosis. | |||||||||||||||
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Transcription factors are also regulated by S-glutathionylation in response to ROS, including p53, AP-1, c-Jun, and NF-kappa B [36]. | |||||||||||||||
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NFAT, C/EBP, Jun and AP-1 transcription factor regulation of LTR activity also have distinct differences in monocyte-macrophages compared to T cells. | |||||||||||||||
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Other up-regulated genes at this time point were the transcription factor Jun and BTG1. | |||||||||||||||
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Moreover, c-jun and junD activity were affected by glucosamine pretreatment in HPCs. | |||||||||||||||
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There is substantial evidence indicating that mitogen-activated protein kinase (MAPK), a family including extracellular signal-regulated protein kinase, p38 MAPK, and c-Jun N-terminal kinase, can be activated by chronic morphine treatment in the central and peripheral nervous systems and that application of a MAPK inhibitor reduces morphine tolerance and dependence. | |||||||||||||||
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A triple function of PLA2-derived lipid mediators has been suggested: causing immediate inflammatory signs, involvement in secondary processes, e.g., superoxide free radical (O2) generation, apoptosis, or tumour necrosis factor-alpha (TNF-alpha)-cytotoxicity, and controlling the expression and activation of pivotal proteins implicated in inflammation and cell development, e.g., cytokines, adhesion proteins, proteinases, NF-kappaB, fos/jun/AP-1, c-Myc, or p21ras. | |||||||||||||||
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The MEK (MAP kinase kinase) and extracellular signal regulated kinases (ERK) pathway primarily responds to cellular proliferation signals, while the p38 MAP kinases and c-Jun N-terminal kinases are modulated by cytokines, growth factors and a variety of cellular stress signals [97]. | |||||||||||||||
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As with the network findings from the entire population of newborns, the networks identified here integrate proteins known to be involved in cell cycle regulation including JUN, as well as stress-response proteins such as interleukin-8 (IL-8), the pro-inflammatory interleukin 1 family member IL1-? | |||||||||||||||
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Therefore, we examined whether these cytokines affected MMP-12 secretion mediated through regulation of c-Jun activity in ASMC. | |||||||||||||||
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Hypoxia can promote lymph node metastasis via up-regulation of PLAUR [39], and up-regulation of HIF1a, JUN and PLAUR in our invasive cell lines hints at possible activation of JUN/AP1 and HIF/ARNT pathways in melanoma (Figure 5). | |||||||||||||||
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The accumulation of cells in G1 was associated with decreased levels of expression of cyclin D1 but no effect was seen on the expression of CDK4 or the immediate early response gene c-jun. | |||||||||||||||
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