INT200900
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Three mitogen-activated protein kinases (MAPKs), including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase, (ERK) and p38 kinase (p38), were investigated using Western immunoblots. | |||||||||||||||
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and JNK, generation and accumulation of ROS and elimination/excretion of As from the body. | |||||||||||||||
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We observed significant increases in the phosphorylation of JNK and ERK (normalized to total protein) in 2CLP monolayers compared to sham (Figure 9). | |||||||||||||||
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JNK is known to phosphorylate many cellular proteins, including several implicated in apoptosis, and can translocate to the nucleus to activate c-Jun and AP-1-mediated gene transcription, leading to transcription of pro-death genes [62]. | |||||||||||||||
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In time course analyses, we examined a panel of transcription factors [18],
[28], [29], and established the kinetics of nuclear accumulation of p-WOX1, c-Jun, ATF3, JNK, NF-? | |||||||||||||||
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The various MAPKs, especially ERK2 and p38 are known to be activated by ACs, and in rare cases (though sometimes reciprocal) even JNK. | |||||||||||||||
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Elk-1 is reportedly down-stream of ERK 1/2, MAPK, and JNK (Fig. 2; Web Appendix) [13, 28]. | |||||||||||||||
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Andrographolide induces apoptosis in human cancer cells via the activation of caspase 8, pro-apoptotic Bcl-2 family members Bax conformational change, release of cytochrome C from mitochondria and activation of caspase cascade [52] and/or via the activation of tumour suppressor p53 by ROS-dependent c-Jun NH2-terminal kinase (JNK) activation, thereby increasing p53 phosphorylation and protein stabilization [53,54]. | |||||||||||||||
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A number of drugs targeting the kinases p38, JNK, MEK, IKK2, JAK3, Lck, and Syk are currently undergoing clinical trials for the treatment of diseases related to inflammation and autoimmunity. | |||||||||||||||
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