IndraLab
Statements
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"JNK is primarily a stress-response pathway and can be activated by proinflammatory cytokines and growth factors coupled to membrane receptors or through non-receptor pathways by stimuli such as heat shock, UV irradiation, protein synthesis inhibitors, and conditions that elevate the levels of reactive oxygen intermediates (ROI)."
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"Possible mechanisms through which FFA mediated NF-B activation and cytokine production can result in insulin resistance includes activation of JNK by cytokines ( xref , xref ) and induction of suppressor of cytokine signaling (SOCS) which can interfere with binding of IRS1/2 to the insulin receptor ( xref )."
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"JNKs can be activated by several growth factors and cytokines and by stress‐inducing signals from pathogens, radiation, and drugs, and their activity is known to influence a number of cellular functions such as differentiation, cell polarity, proliferation, and viability (Wagner & Nebreda, xref ; Hotamisligil & Davis, xref )."
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"P38 MAPK and c-Jun N-terminal kinase (JNK), two members of the MAPK superfamily, are activated by cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, or G protein-coupled receptors, and have an important role in inflammation and apoptosis in response to stress ( xref )."
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"Taken together, HBV or HCV components and pro-inflammatory cytokine additively activate JNK to shift Smad phospho-isoform signaling from the tumor-suppressive TβRI/pSmad3C pathway to the carcinogenic JNK/pSmad3L pathway together with the fibrogenic pSmad2L/C pathway, accelerating liver fibrosis and promoting hepatocarcinogenesis."
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"TNF-α and other inflammatory cytokines activate JNK and ERK. xref , xref TNF-α is generated by Kupffer cells, endothelial cells, and T cells, among others. xref , xref It functions not only as a proinflammatory factor but also as a proapoptotic factor. xref TNF-α can strongly activate JNK and ERK, followed by the phosphorylation of Bcl-2."
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"Alterations of MAPKs′ play a major role in the development and progression of RCC.[ xref ] The JNK predominantly activated by cytokines,UV radiation, growth factor deprivation,DNA-damaging agents, and certain G-protein coupled receptors.[ xref ] JNK activation has been demonstrated in several glomerulonephrities and JNK inhibition suppresses inflammation in rat antiglomerular basement membrane disease.[ xref xref ] An et al .[ xref ] described that the blockade of JNK activation provokes reduced growth and motility of RCC cells in vitro and in vivo."
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"Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases that regulate a variety of cellular processes including proliferation, inflammation, invasion and apoptosis. xref , xref The mammalian extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinase (JNK) and p38 kinase are three major MAPK families that are activated by a wide range of stimuli. xref ERK is primarily activated by growth factors, whereas JNK and p38 are activated by cytokines and stresses. xref , xref Upon stimulation, MAPKs activate cytosolic or nuclear-localized effector molecules and thereby translate the stimulus into a cellular response. xref , xref , xref The MAPKs are the executor kinases in a three-tiered kinase-signaling cascade."
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"Mutationally activated Rac1 potently and selectively activates JNK without affecting MAPK and dominant negative mutants of Rac1 block the JNK activation induced by cytokines and growth factors in COS-7 cells, suggesting that Rac1 plays a critical role in controlling the JNK signaling pathway [ xref ]."
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"Previous reports reviewed that p38 and p44/42 MAPKs may play a critical role in harmful microglial activation in acute brain injury [ xref ]; JNK is activated by proinflammatory cytokines and cellular stress, and play essential roles in regulating inflammatory responses [ xref , xref ]; activation of MAPK entities, especially Erk and p38, is a determinant of neuronal survival on certain occasions [ xref - xref ]; and, selective inhibitors (PD98059 and SB203580) are candidates for treatment [ xref , xref ]."
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"Therefore, we concluded that the JNK signaling cascade plays an important role not only in stress responses and proinflammatory cytokine actions but also in hematopoietic cytokine actions and that hematopoietic cytokines may activate the JNKs through a kinase other than SEK1/MKK4, as previously suggested for stress-activated cells."