IndraLab

Statements


| 141

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"Activation of JNK by cytokines and/or oxidative stress may lead to phosphorylation of c-Jun and c-Fos, which heterodimerize to form the Activator Protein-1 complex [ xref ]."

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"However, gene knockout studies revealed that MEKK1 regulates stress-induced JNK activation but is not essential for proinflammatory cytokine-induced activation of JNK and IKK [ xref , xref ]."

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"Interestingly, GCK can be activated by TNF, suggesting that GCK could mediate JNK activation by cytokines."

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"Namely, activation of ERK contributes to cell differentiation, proliferation and survival, whereas JNK and p38 are activated by pro-inflammatory cytokines and environmental stresses and promote apoptosis [ xref ]."

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"Indeed, the addition of the cytokines to the RIN-m5F cell culture medium led to the activation of the JNK signaling cascade, while the addition of PRDX6 completely blocked the cytokine-induced JNK activation in β cells."

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"Taken together, AAT significantly improves islet graft survival after intraportal islet transplantation by mitigation of coagulation in IBMIR and suppression of cytokine-induced JNK and NF-κB activation."

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"Cytokine-induced JNK activation is abolished in MKK7-deficient mast cell ( xref , xref )."

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"Reactive oxygen species mediate cytokine activation of c-Jun NH2-terminal kinases."

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"MKK7 is specifically associated with cytokine-induced JNK activation, through phosphorylation of the Thr residue of JNK xref ."

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"JNK is activated by various cytokines and environmental stresses, and it subsequently regulates phosphorylation of c-Jun and AP-1 transcription activity [ xref ]."

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"Inflammation-mediated IR implicates several pathways including IKKβ/NF-κB, JNK and SOCS3, which are activated by inflammatory cytokines."

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"JNK and p38 were not activated by any of the other cytokines and growth factors tested."

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"Notably, although JNK activation by proinflammatory cytokines was completely abolished in TAK1-deficient cells, the IKK activity was mostly but not completely blocked, suggesting that a TAK1-independent mechanism may contribute to the residual activation of IKK."

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"Understanding the mechanisms by which steady laminar flow regulates JNK activation by cytokines may provide insight into the atheroprotective mechanisms induced by laminar blood flow."

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"Cellular stress induced by viral infection, bacterial toxins, and proinflammatory cytokines strongly activates JNKs ( xref )."

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"While ERK is considered to be strongly associated with cell proliferation, JNK is strongly activated by certain cytokines and cellular stress (Su and Karin, 1996; Yang et al., 1998) ."

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"What is the role of cytokine-induced JNK activation?"

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"Both JNK and p38 MAPK are preferentially activated by inflammatory cytokines and cellular stresses instead of classic mitogenic stimuli ( xref , xref )."

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"In various cell types, JNK is preferentially activated by cytokines (IL-1β and tumor necrosis factor α) or stress stimuli such as osmotic shock, UV light and heat."

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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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"The c-Jun NH2-terminal kinase was activated by cytokines, but the most efficacious cytokine was tumour necrosis factor-alpha which did not induce NOS II by itself."

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"JNKs and p38 are activated by inflammatory cytokines and environmental stressors to regulate inflammation, apoptosis, and differentiation [ xref ]."

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"The latter involves activation of JNK and c-Jun by inflammatory cytokines, Reactive oxygen species (ROS), mixed lineage kinases, radiation or excitotoxicity [ xref ]."

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"Stress conditions and proinflammatory cytokines activate the c-Jun NH2-terminal kinase (JNK), a member of the stress-activated group of mitogen-activated protein kinases (MAPKs)."

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"Similar to NF- KB, cytokine activation of JNKs has been demonstrated to be regulated by redox-dependent processes."

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"Moreover, JNK and p38 are mainly activated by pro-inflammatory cytokines in response to stress, while ERK is induced by growth-promoting mitogenic stimuli [ xref ]."

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"In addition, the activation of JNK by cytokines, inflammatory mediators, and fatty acids phosphorylate IRS-1, modifying insulin signaling."

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"Another mechanism that might be related to corticosteroid resistance, is the activation of c-Jun N-terminal kinase (JNK) by pro-inflammatory cytokines leading to phosphorylation of GR at Ser226 and prevention of binding to GRE."
| PMC

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"Downregulation of MEKK-1 in human islet cells provoked opposite effects, i.e., attenuation of cytokine-induced JNK and MKK4 activation, IkappaB stability, and a less pronounced NF-kappaB translocation."

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"PPAR-γ agonists have been shown to inhibit cytokine-induced activation of JNK in an insulinoma cell line [ xref ]."

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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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"Cytokine-induced JNK activation is dependent on MKK7 in cultured FLS and does not require MKK4."

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"JNK activation by inflammatory cytokines and FFA was shown to be a major contributor to obesity-induced insulin resistance and metabolic inflammation [ xref , 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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"Furthermore, JNK and p38 MAPK signalling molecules are predominantly activated depending upon the inflammatory cytokines and environmental stress, which ultimately helps in cell differentiation and apoptosis [ 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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"One possibility might be that IL-15 but not IL-2 induces another cytokine that can activate JNK and take the relay of IL-15."

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"C-Jun N-terminal kinase (JNK) is activated by oxidants and cytokines and regulates hepatocellular injury and insulin resistance, suggesting that this kinase may mediate the development of steatohepatitis."

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"Jnks are activated by growth factors and cytokines that stimulate cell motility, and this often requires upstream activation of Rho GTPases."

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"Rapid activation of JNK by cytokines, such as IL-1, has been reported to participate in cytokine-induced β-cell apoptosis, possibly during prolonged activation of ER stress pathways in islets. xref , xref – xref Nitric oxide also activates JNK."

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"Prolonged upregulation of a stressed UPR induces apoptosis, a process that involves JNK activation by the pro-inflammatory cytokines that act upon pancreatic β-cells through the progression of diabetes."

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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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"For example, simultaneous disruption of both Mkk4 and Mkk7 genes was required to block JNK activation by UV or anisomycin, whereas disruption of Mkk7 alone was sufficient to prevent JNK activati[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"JNK is primarily activated by proinflammatory cytokines and stress by being phosphorylated by MAP3Ks, including ASK1 and TAK1 [ xref , xref ]."

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"In the present study, Spirulina extract attenuated the cytokine-induced activation of JNK and p38 kinase in RINm5F cells, further demonstrating a protective effect against oxidative stress."

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"ERKs are known to be activated by growth factors and mitogens, whereas cellular stresses and inflammatory cytokines activate JNKs and p38s [ xref ]."

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"Pro-inflammatory cytokines that are overexpressed in states of obesity activate JNK through the actions of the MKPs that are inactivated as a result of increased levels of reactive oxygen species [ xref ]."

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"Activation of JNK and IKK by these cytokines requires the kinase activity of TAK1, which is activated by TRAF2 or TRAF6, two RING domain ubiquitin ligases that catalyze the synthesis of polyubiquitin chains linked via a lysine at position 63 (K63)."

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"JNK and p38 are activated by various inflammatory cytokines and environmental stressors and they play important roles in apoptosis and cytokine production."

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"Interestingly, PKCepsilon RNAi depletion significantly enhanced the release of TNFalpha in response to PMA and greatly potentiated JNK activation by this cytokine."

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"Cellular JNKs are activated by cytokines (e.g., TNF, IL-1) and by exposure to environmental stresses (e.g., osmotic stress, redox stress, radiation) ( xref )."

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"In insulin-secreting cells, cytokines activate the c-Jun N-terminal kinase (JNK), which contributes to a cell signaling towards apoptosis."

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"These cytokines activate JNK and STAT3, promoting the transcription of apoptotic-, inflammation-, proliferation-, differentiation- and angiogenesis-related genes."

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"Similar to insulin, the activation of JNK and IKKβ/NFκB by proinflammatory cytokines also leads to reduced leptin signaling [ xref ]."

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"JNK is activated by inflammatory cytokines, free fatty acids, cigarette smoke, and nicotine xref ."

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"ERKs are predominantly activated by mitogenic factors, while JNK and p38 are preferentially activated by proinflammatory cytokines and stress-inducing stimuli [ xref ]."

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"These results demonstrated that clathrin-dependent endocytosis is required for the inhibitory effect of AAT on cytokine-induced JNK pathway activation."

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"Thus, after intra-tibial inoculation with carcinoma cells, it is probable that the increased release of proinflammatory cytokines induced JNK activation in the spinal cord."

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"Broadly, growth factors and mitogens activate ERK1/2 and ERK5, while cellular stress signals and inflammatory cytokines activate both JNK and p38 [ xref , xref ]."

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"The mammalian mitogen-activated c-Jun N-terminal kinases (JNKs) can be activated by cytokines or environmental stress and are known to regulate processes including development and cell survival [ xref ]."

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"Several studies have demonstrated that p38 MAPK and JNK are activated by ROS or pro-inflammatory cytokines and promote apoptosis [ xref – xref ]."

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"JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands."

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"It was reported that JNK in fibroblasts could be activated by cytokines and then regulate the production of IL-6 []."

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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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"While over-expression of dominant inhibitory Rac can block JNK activation by cytokines such as TNF and IL-1 , lower doses preferentially block JNK activation by growth factors but not TNF (and Liu and[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"C-Jun N-terminal kinase (JNK) and p38 MAPKs are activated by inflammatory cytokines or environmental stress."

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"Somewhat differently, CO was shown in Caco-2 cells (an adenocarcinoma line), to decrease cytokine-induced activation of p38 MAPK, JNK and ERK1/2 as well as NF-κB, xref ."

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"In contrast, cytokine-induced JNK1/2 phosphorylation was not significantly altered by PBA treatment ( xref ), suggesting that ER stress is not required for cytokine-induced JNK activation."

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"C-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase (MAPK) family, is activated by specific cytokines and various environmental stresses."

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"Previously, we have shown that JNK pathway minimally, if any, contributes to TNFα-stimulated Fra-1 transcription in A549 cells, despite a high level of JNK activation by this pro-inflammatory cytoki[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In addition, transfection of a RhoGAP, which inactivates all Rho family members, reduces activation of JNK by cytokines, and transfection of Dbl or Ost, GDSs for Cdc42 and also RhoA, efficiently activ[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Proinflammatory cytokines such as TNF-α and IL-1β activate JNK and IKKβ/NF-κB through classical receptor-mediated mechanisms which are also activated by pattern recognition receptors, bound to substances as lipopolissacharide (LPS) from gram negative bacteria."

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"JNK in fibroblasts could be activated by inflammatory cytokines or double-stranded viral RNA and then regulated the production of type I interferon and interleukin-6 (IL-6) []."

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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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"C-Jun N-terminal kinases (JNK) are activated by inflammatory cytokines and have a key role in beta-cell apoptosis and in negative regulation of insulin signaling."

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"JNK is activated by proinflammatory cytokines, environmental stress (e.g., hypoxia, UV and g-radiation, heat shock, redox stress, etc.) or several cytotoxic drugs."

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"Conversely, sustained activation of NF-kappaB inhibits cytokine-induced JNK activation."

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"In addition, JNK could be activated by proinflammatory cytokines, growth factors and immune cells favoring tumor development [ xref , xref , xref ]."
| PMC

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"Cellular stress induced by viral infection, bacterial toxins, and proinflammatory cytokines strongly activates JNKs (Lee et al., 2016)."

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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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"Additionally, we had shown that rosiglitazone treatment improves the survival of insulin-secreting cells lines exposed to the proinflammatory cytokine IL-1β concomitantly with the inhibition of the cytokine-induced activation of JNK ( xref )."

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"C-Jun N-terminal kinase (JNK; including JNK1, JNK2 and JNK3 isoforms) is associated with insulin resistance and is activated by inflammatory cytokines and free fatty acids (FFAs), which are associated with type 2 diabetes ( xref , xref , xref )."

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"13,19 MAP2K4 deletion is sufficient to block JNK activation by inflammatory cytokines."

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"ERKs can be stimulated by mitogens, while JNK and p38 MAPK can be activated by heat shock proteins and inflammatory cytokines [ xref ]."

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"JNK can be activated by many inflammatory cytokines and environmental factors [ xref , xref , xref ]."

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"The stress kinases p38 and JNK are generally activated by inflammatory cytokines and different stressors, including DNA-damaging compounds [ xref ]."

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"ERK1/2 is activated 393 by growth and neurotrophic factors (54-56); JNK and p38 MAPK are activated by 394 inflammatory cytokines and by a wide variety of cellular stresses (57, 58)."
| DOI

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"Both FFA and the pro-inflammatory cytokines can activate c-Jun N-terminal kinase (JNK), leading to increased phosphorylation of interferon regulatory factor 3 (IRF3) and in this way contributing to the reduced UCP1 expression and WAT browning [ xref ]."
| PMC

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"It is known that stimulation by ultraviolet radiation or pro-inflammatory cytokines rapidly activates c-Jun N-terminal kinase (JNK) and induces the phosphorylation of ATF-2, which is necessary for its[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Incubation of HUVEC with PD98059, which inhibits flow-mediated ERK1/2 activation, prevented flow from inhibiting cytokine activation of JNK."

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"TUDCA also protected islet cells from cytokine-induced JNK activation and apoptosis (274)."

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"Our previous study showed that alpha-1 antitrypsin (AAT) inhibits β cell death through the suppression of cytokine-induced c-Jun N-terminal kinase (JNK) activation in an islet transplantation model."

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"In addition, JNK is strongly activated by cytokines such as Tumor Necrosis Factor a (TNF) and Interleukin-1 (IL-1) ."

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"More apropos for the present study however, JNK is activated by inflammatory cytokines, and free fatty acids, both of which are elevated in hypercholesterolemia-driven development of atherosclerosis [ xref ]."

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"These observations are consistent with a previous finding that proinflammatory cytokine-activated JNK also contributes to γ-secretase activity and Aβ production in HEK293 cells ( xref )."

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"Macrophage cytokines activated ERK and JNK in PIN cells."

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"Broadly, growth factors and mitogens activate ERK1/2 and ERK5, while cellular stress signals and inflammatory cytokines activate both JNK and p38 [58,59]."

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"JNK, which is activated by environmental stress, phosphorylates and regulates the activity of transcription factors including c-Jun. Moreover, JNK is also activated by proinflammatory cytokines, such as TNF and IL-1 [ xref ]."

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"Cytokine-induced JNK activation is strictly dependent on the mitogen-activated protein kinase kinase 7 (MKK7) in fibroblast-like synoviocytes (FLS)."

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"Obesity and the associated inflammatory state in insulin-responsive tissues result in the release of pro-inflammatory cytokine that activates the stress-responsive MAPKs, p38 MAPK, and JNK."

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"Meanwhile, through TNFR2, this cytokine activates c-Jun N-terminal kinase (JNK), but not MAPK or p38 MAPKs signaling pathways, and its function is linked to enhance apoptotic cell death [ xref ]."

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"Except ROS, JNK can also be activated by some pro-inflammatory cytokines including TNF and IL-1 [ xref ]."

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"MEKK1 associates with the RING–zinc finger domain of TRAF2 and TRAF6 upon TNF and IL-1 stimulation, respectively, and a dominant negative mutant of MEKK1 interferes with JNK activation by these cytoki[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"We observed that overexpression of wild-type MEKK-1, but not of a kinase dead MEKK-1 mutant, resulted in potentiation of cytokine-induced JNK activation, inhibitor of kappaB (IkappaB) degradation, and cell death."

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"JNK is activated by proinflammatory cytokines and mediators, and plays a crucial role in immune system signaling ( xref )."

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"In the present study, we provide evidence of differential signaling mechanisms for the activation of JNK by palmitate and cytokines."

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"The effect of TF/FVIIa on cytokine-induced beta cell death was found to be dependent on the stress kinase JNK, since FVIIa addition potentiated cytokine-induced JNK activation and JNK inhibition abolished the effect of TF/FVIIa on cytokine-induced beta cell death."

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"Previous studies have demonstrated that fluid shear stress (flow) inhibits cytokine-induced JNK activation in endothelial cells (ECs)."

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"The finding that JNK and p38 are strongly activated by pro-inflammatory cytokines such as TNF and IL-1, suggests that these signaling pathways may also have a role in inflammatory responses."

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"We have previously reported that TZDs, in a PPARγ-dependent manner, are able to inhibit obesity- and proinflammatory cytokine–induced activation of JNK and, in doing so, alleviate insulin resistance ( xref )."

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"TβRI activates Smad3 to create COOH-terminally phosphorylated Smad3 (pSmad3C), while pro-inflammatory cytokine-activated JNK phosphorylates Smad3 to create the linker phosphorylated Smad3 (pSmad3L) [ xref ]."

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"JNK is usually activated by stress cytokines such as IL-1α and TNF-α [ xref ]."

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"JNK is activated by inflammatory cytokines, such as interleukin 1 and tumor necrosis factor, osmotic and heat stresses , and UV irradiation ."

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"On the other hand, JNK and p38 MAP kinase are activated by various inflammatory cytokines and environmental stressors, and play an important role in the signal cascades leading to the induction of cytokines and chemical mediators ( xref )."

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"Previous studies ( xref ) show that MKK4 is important for stress-induced activation of JNK, whereas MKK7 is involved in inflammatory cytokine-induced activation of JNK."

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"Furthermore, these two cytokines also activated JNK, especially in CCL2-treated Pr111 cells."

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"Subsequent studies have shown that JNKs can also be activated by growth factors as well as inflammatory cytokines [ xref , xref - xref ]."

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"Among the MAPKs, the JNKs are generally activated by cytokines, UV irradiation, destitution of growth factor, and DNA damage [ xref ]."

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"Surprisingly, cytokine-induced JNK activation and MMP production are strictly dependent on MKK7 in cytokine-stimulated FLS and do not require MKK4 [ xref ]."

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"We have also evaluated the activation level of JNK which is activated by inflammatory cytokines and free fatty acids in db / db mice [ xref ]."

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"Like IL-1, IL-18 or IL-33, IL-36 cytokines activate nuclear factor (NF)-κB, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK)-1/2 intra-cellular signaling pathways upon receptor binding [ xref ]."

sparser
"Lung ECs showed activation of Rho kinase, a signaling molecule that is important for regulating EC permeability increases and JNK activation induced by inflammatory cytokines ( xref )."

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"This amplification might be based on the synergistic/additive activation of signal transducer and activator of transcription 3 and c-Jun N-terminal kinase by both cytokines ( Supplementary Figure S1 o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Although JNK and p38 are coordinately activated by proinflammatory cytokines, environmental stresses, and hematopoietic cytokines [22–24] , only p38 appears to be responsible for the phosphorylation [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In addition, the activation of JNK by inflammatory cytokines or by stress is frequently accompanied by the nuclear translocation of NF- κ B, and many genes require the concomitant activation of AP-1 and NF- κ B [ 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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"Cytokine-induced JNK activation has also been implicated in decreased GSIS by suppressing the IRS/PI3K/Akt signaling pathway ( xref ; xref ; xref ; xref ; xref )."

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"In hOAC, JNK is mainly activated by proinflammatory cytokines such as IL-1 and tumor necrosis factor (TNF)-α."

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"Meanwhile, JNK is activated by pro-inflammatory cytokines, ultraviolet irradiation, heat, and osmotic shock, which inhibit proliferation and induce apoptosis."

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"JNK are usually activated by inflammatory cytokines and environmental stresses, including UV irradiation, osmotic stress, redox stress, and mechanical stress 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."

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"Furthermore, hGSTA1-1 suppresses JNK signaling activation by proinflammatory cytokine and oxidative stress, suggesting a potential protective role of hGSTA1-1 against JNK [ xref ]."
| PMC

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"JNK is activated primarily by cytokines or exposure to environmental stresses such as UV irradiation."

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"ERKs are activated by mitogens and growth factors, whereas JNK and p38 are activated by inflammatory cytokines (IL-1 and TNF-α), cellular stress (heat and osmotic), reactive oxygen species, and ultraviolet irradiation [ xref – xref ]."

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"In various cell types, JNK is preferentially activated by cytokines (IL-1β and TNFα) or stress stimuli such as osmotic shock, UV light and heat [9,24] , and JNK participates in cell proliferation as [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"For instance, the expression of the dominant negative MAP3K1 blocks the activation of JNK and/or ERK by inflammatory cytokines such as TNFα and INFγ [ xref , xref ]."

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"JNK can be activated by inflammatory cytokines and numerous stressors such as heat shock, oxidative stress, or DNA damage, which follow I/R [ xref – xref ]."

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"ERK1/2 are activated by mitogens and growth factors leading to cell growth and survival, whereas JNK and p38 MAPK are preferentially activated by pro-inflammatory cytokines and oxidative stress resulting in cell differentiation and apoptosis [ xref ]."

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"Several studies reported that inflammatory cytokines activate JNK, resulting in the switch in Smad3 signaling from tumor-suppression to oncogenesis [ xref – xref ]."

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"Subsequently, a second vertebrate stress-activated MAP kinase subfamily was discovered, now generally referred to as p38 [16,17] , which like JNK is activated potently by inflammatory cytokines and s[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"