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Human JNK Protein expressed in Baculovirus infected Insect Cells - ABIN593493
Sury, McShane, Hernandez-Miranda, Birchmeier, Selbach et al.: Quantitative proteomics reveals dynamic interaction of c-Jun N-terminal kinase (JNK) with RNA transport granule proteins splicing factor proline- and glutamine-rich (Sfpq) and non-POU ... dans Molecular & cellular proteomics : MCP 2015
Human JNK Protein expressed in Wheat germ - ABIN1310303
Prause, Christensen, Billestrup, Mandrup-Poulsen: JNK1 protects against glucolipotoxicity-mediated beta-cell apoptosis. dans PLoS ONE 2014
These results provide the first evidence for the anticancer potential of Piperine in ovarian cancer cells, partially via JNK/p38 MAPK-mediated intrinsic apoptotic pathway
TMEM88 plays a significant role in TNF-alpha-enhanced cytokine (IL-6 and IL-1beta) secretion of LX-2 cells via regulating JNK/P38 and canonical Wnt/beta-catenin signaling pathway.
High JNK1 expression is associated with prostate cancer.
results revealed that melatonin attenuated chemokine CCL24 levels through inhibition of the JNK pathway to hinder human osteosarcoma cell invasion, thereby highlighting the therapeutic potential of melatonin for osteosarcoma metastasis.
JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.
Data show that overexpression of protein-tyrosine phosphatase 1B (PTP1B) activated the c-Jun N-terminal kinase (JNK) signaling pathway.
HMBG2 overexpression promotes ischemia/reperfusion-induced cell apoptosis through activating the JNK1/2-NF-kappaBp65 signaling in AC16 cardiomyocytes.
JNK1 and VDR act as tumor suppressors, and their stromal expression levels are associated with prognosis in esophageal squamous cell carcinoma.
These findings further validated the involvement of P. acnes in the pathology of intervertebral disc degeneration (IVDD) and provided evidence that P. acnes-induced apoptosis of NPCs via the TLR2/JNK pathway is likely responsible for the pathology of IVDD.
CXCL12 activates the MEKK1/JNK signaling pathway, which in turn initiates SMAD3 phosphorylation, its translocation to nuclei, and recruitment of SMAD3 to the CTGF promoter, which ultimately induces CTGF expression in human lung fibroblasts.
Activation of the c-Jun NH2-terminal kinase pathway by coronavirus infectious bronchitis virus promotes apoptosis independently of c-Jun.
Inhibition of each TGFbeta receptor-I, glucocorticoid receptor or JNK signaling partially reversed the dexamethasone-mediated effects, suggesting a complex signaling network. These data reveal that dexamethasone mediates progression by membrane effects and binding to glucocorticoid receptor
JNK inhibitor prevents SIRT1 phosphorylation, leading to elevated SIRT1 protein levels even in the presence of H2O2. Taken together, our results indicate that CHFR plays a crucial role in the cellular stress response pathway by controlling the stability and function of SIRT1.
Findings suggest that during lipoapoptosis, HCV infection may enhance hepatocyte toxicity by increasing JNK phosphorylation.
High JNK expression is associated with non-small-cell lung cancer.
These data suggested that Annexin A2 induces cisplatin resistance of non-small cell lung cancer (NSCLC)via regulation of JNK/c-Jun/p53 signaling, and provided an evidence that blockade of Annexin A2 could serve as a novel therapeutic approach for overcoming drug resistance in NSCLCs
Data suggest that H2O2 regulates cell death in granulosa cells via the ROS-JNK-p53 pathway.
High expression of JNK is associated with invasion of gastric cancer.
JNK activation and signaling in extrahepatic cholangiocarcinoma is regulated by L1CAM.JNK role in cell migration in extrahepatic cholangiocarcinoma.
Thus, the present study indicated that parkin knockout inhibits neural stem cell differentiation by JNK-dependent proteasomal degradation of p21.
Thus, Bifidobacterium longum BB68 increased the longevity of nematodes by activating the TIR-1 - JNK-1 - DAF-16 signaling pathway, and the cell wall component of BB68 contributed to longevity.
responsible for the immune response elicited by the host during the Shigella flexneri infection
Findings indicate the MIG-15/JNK-1 pathway can restrict both glutamatergic synapse formation and short-term learning.
Our genetic study unravelled the underlying pathway where JNK-1 is acting independently of insulin-IGF-1 signalling (IIS) pathway to modulate longevity. In support of in vivo results in silico docking study of UA with C. elegans JNK-1 ATP-binding site suggested promising binding affinity exhibiting binding energy of -8.11 kcalmol(-1). UA induced JNK-1 activation in wild-type animals underlie the importance of pharmacologi
JNK-1 directly interacts with and phosphorylates DAF-16. Moreover, in response to heat stress, JNK-1 promotes the translocation of DAF-16 into the nucleus.
The present study shows in Caenorhabditis elegans that ambient temperature (1-37 degrees C) specifically influences the activation (phosphorylation) of the MAP kinase JNK-1 as well as the nuclear translocation of DAF-16.
the stress response is controlled by a c-Jun N-terminal kinase (JNK)-like mitogen-activated protein kinase (MAPK) signaling pathway, which is regulated by MLK-1 MAPK kinase kinase (MAPKKK), MEK-1 MAPK kinase (MAPKK), and KGB-1 JNK-like MAPK.
The results reported herein support a role of JNK/c-Jun activation in apoptosis but suggest that it is not primarily responsible for Bax-dependent events, such as mitochondrial ROS production and cytochrome c release, in apoptotic sympathetic neurons isolated from mice
In conclusion, the activation of JNK and p38 after cerebral ischemia caused an increase in cerebral SGLT-1. The regulation of cerebral SGLT-1 expression via the MAPK pathway may be a novel therapeutic strategy for cerebral ischemia patients.
JNK1 and/or JNK3 are promising targets for the prevention of cell death and inflammation during epileptogenesis.
The up-regulation of HMGB1 was thought to be modified by dual channels: in the transcriptional level, it was regulated by JNK1/JNK2-ATF2 axis; post-transcriptionally, it was regulated by the microRNA (miR)-200 family, especially miR-429. miR-429 liver conditional knockout mice (miR-429(Deltahep)), fed either a normal diet or an HFD, showed severe liver inflammation and dysfunction, accompanied by greater expression of ...
Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation.
Prdx1 knockout can aggravate the oxidative stress and lung injury by increasing the level of Reactive Oxygen Species (ROS), and also activate P38/JNK signaling pathway.
Data identify a unique signal crosstalk between Wnt signaling and the MAP3K1-JNK pathway in epithelial morphogenesis.
Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668.
These interactions are required for SRC-induced activation of VAV and the subsequent engagement of a JIP1-tethered JNK signaling module.
this study establishes that JNK1 is a key mediator of osteoblast function in vivo and in vitro.
Jnk1 deficiency inhibits the development of neural stem cells/precursors
Suppressing P38 promoted adipogenic trans-differentiation and intensified adipolytic metabolism in differentiated cells. However, inhibition of ERK1/2 had the opposite effects on adipogenesis and no effect on adipolysis. Blocking JNK weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis.
the effects of JNK1 deficiency in an experimental model of familial Alzheimer's disease, was investigated.
Irradiation coupled with JNK inhibition in beta1 integrin -/- transgenic adenocarcinoma of prostate (TRAMP) leads to increased levels of nuclear focal adhesion kinase (FAK) in tumor cells.
transgenic mice overexpressing sPLA2 -IIA keratinocytes showed enhanced activation of EGFR and JNK1/2 that led to c-Jun activation.
p53 plays a novel protective role in APAP induced liver injury through inhibiting the activation of JNK, a key mediator in APAP-induced oxidative stress.
We crossed Ptf1a(Cre/+) ;Kras(G12D/+) mice with JNK1(-/-) mice to generate Ptf1a(Cre/+) ;Kras(G12D/+) ;JNK1(-/-) (Kras;JNK1(-/-) ) mice. Tumor weight was significantly lower in Kras;JNK1(-/-) mice than in Kras;JNK1(+/-) mice, whereas histopathological features were similar.we concluded that inhibition of activated JNK in pancreatic tumor stroma could be a potential therapeutic target to increase Ccl20 secretion
BOC interacts with ABL and activates JNK thereby promoting neuronal differentiation and neurite outgrowth.
JNK and Yorkie cooperatively drive tumor progression by generating oncogenic polyploid giant cells.
provide a mechanism to explain how an ATF3-Raw module controls JNK signalling to maintain normal intestinal barrier function during acute infection
Cell fusion during wound healing in Drosophila larval epidermis occurred primarily in the wound vicinity, where JAK/STAT activation was suppressed by fusion-inducing JNK signaling.
aken together, these results reveal that inactivation of Rpd3 independently regulates JNK and Yki activities and that both Hippo and JNK signaling pathways contribute to Rpd3 RNAi-induced apoptosis.
Increased expression of the Drosophila JNK basket in the setting of reduced cindr expression was found to result in even more severe apoptosis, whilst ectopic death was found to be reduced if retinas were heterozygous for basket.
Data show that JNK signalling inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner cell proliferation.
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr) pathway in the lateral epidermis for sustained dpp expression in the LE. Specifically, we demonstrate that Egfr pathway activity in the lateral epidermis prevents expression of the gene scarface (scaf), encoding a secreted antagonist of JNK signaling
n addition to significantly increasing the number of JNK target genes identified so far, our results reveal that the LE is a highly heterogeneous morphogenetic organizer, sculpted through crosstalk between JNK, segmental and AP signalling. This fine-tuning regulatory mechanism is essential to coordinate morphogenesis and dynamics of tissue sealing
malignant transformation of the ras(V12)scrib(1) tumors requires bZIP protein Fos, the ETS-domain factor Ets21c and the nuclear receptor Ftz-F1, all acting downstream of Jun-N-terminal kinase.
Diminished MTORC1-dependent JNK activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
correct Cindr-dJNK stoichiometry is essential to maintain epithelial integrity and disturbing this balance may contribute to the pathogenesis of disease states, including cancer
ROS/JNK/p38/Upd stress responsive module restores tissue homeostasis. This module is not only activated after cell death induction but also after physical damage and reveals one of the earliest responses for imaginal disc regeneration.
Significantly, the JNK pathway is responsible for the majority of the phenotypes and transcriptional changes downstream of Notch-Src synergy.
This study demonstrated that the mechanism by which Bsk is required for pruning is through reducing the membrane levels of the adhesion molecule Fasciclin II (FasII)
Study solves the crystal structure of unphosphorylated DJNK in complex with adenylyl imidodiphosphate (AMP-PNP) and magnesium.
PERK/ATF4 activated the JNK pathway through Rac1 and Slpr activation in apoptotic cells.
Data show that oxidative stress and neuroinflammation are intrinsic components of TDP-43-associated neurodegeneration and the balance between cytoprotective JNK and cytotoxic p38 signaling dictates phenotypic outcome to TDP-43 expression in Drosophila.
Data show that the actin-Capping Protein (CP) alphabeta heterodimer, which regulates actin filament (F-actin) polymerization, limits Src-induced apoptosis or tissue overgrowth by restricting JNK activation.
In a genetic screen, we identified signaling by the EGFR pathway as important for apoptosis-induced proliferation acting downstream of JNK signaling
A molecular mechanism linking JNK activity to Yki regulation. JNK can promote YAP activity in mammalian cells.
Porcine reproductive and respiratory syndrome virus -activated TAK-1 was essential for the activation of JNK and NF-kappaB pathways and IL-8 expression.
Data show that proinflammatory cytokines induction was ERK1/2 and JNK1/2 dependent.
These data suggest that the p38 and JNK signaling pathways play pivotal roles in PRRSV replication and may regulate immune responses during virus infection.
based on the data, we can conclude that JNK plays an active role in fragmentation of pig oocytes and that p38 MAPK is not involved in this process
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries.
PP2A and AIP1 cooperatively induce activation of ASK1-JNK signaling and vascular endothelial cell apoptosis.
Phorbol 12-myristate 13-acetate activation of ERK and JNK signaling is relevant in the regulation of gene expression during follicular development, ovulation, and luteinization.
study reports MPK8 connects protein phosphorylation, Ca(2)+ and ROS in wound-signaling pathway; suggests 2 major activation modes, Ca(2)+/CaMs and MAP kinase phosphorylation cascade, converge at MPK8 to monitor or maintain an essential part of ROS homeostasis
The results of this study suggest that JNK has a role in the disassembly adherens junctions by means of endocytosis that is required during buccopharyngeal membrane perforation.
Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3-dependent Proteolysis of JNK1-2 and Bid.
JNK signaling is required to establish microtubule stability and maintain tissue cohesion in the gut.
Data show that the death pathway is independent of ERK but relies on activating Bad phosphorylation through the control of both kinases Cdk1 and JNK.
our data provide strong evidence that Jip3 in fact serves as an adapter protein linking these cargos to dynein
P38 and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
A dorsalization pathway that is exerted by Axin/JNK signaling and its inhibitor Aida during vertebrate embryogenesis, is defined.
JNK-Mmp13 signaling pathway plays an essential role in regulating the innate immune cell migration in response to severe injury in vivo
Suggest that hypoxia-induced modified cells engage the PDGFbeta-R-JNK1 axis to confer distinctively heightened proliferation and adventitial remodelling in pulmonary hypertension.
These data suggest a differential requirement of JNK1 and p38 MAPK in TNF regulation of E2F1. Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF-mediated EC dysfunction.
PKD is a critical mediator in H2O2- but not TNF-induced ASK1-JNK signaling
ATF3 induction by acute hypoxia is mediated by nitric oxide and the JNK pathway in endothelial cells
JNK plays an important role in the induction of apoptosis in transformed bovine brain endothelial cells stimulated by LPS
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various cell stimuli, and targets specific transcription factors, and thus mediates immediate-early gene expression in response to cell stimuli. The activation of this kinase by tumor-necrosis factor alpha (TNF-alpha) is found to be required for TNF-alpha induced apoptosis. This kinase is also involved in UV radiation induced apoptosis, which is thought to be related to cytochrom c-mediated cell death pathway. Studies of the mouse counterpart of this gene suggested that this kinase play a key role in T cell proliferation, apoptosis and differentiation. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.
JUN N-terminal kinase
, MAP kinase 8
, c-Jun N-terminal kinase 1
, mitogen-activated protein kinase 8 isoform JNK1 alpha1
, mitogen-activated protein kinase 8 isoform JNK1 beta2
, stress-activated protein kinase 1
, stress-activated protein kinase 1c
, JNK1 beta1 protein kinase
, MAPK 8
, mitogen activated protein kinase 8
, protein kinase mitogen-activated 8
, stress-activated protein kinase JNK1
, SAPK gamma
, c-jun NH2-terminal kinase
, p54 gamma
, JUN kinase
, Jun N-terminal kinase
, Jun NH2-terminal kinase
, Jun-N-terminal kinase
, c-Jun N-terminal kinase
, c-Jun aminoterminal kinase
, c-Jun-N-terminal kinase
, drosophila JNK
, janus kinase 1
, mitogen-activated protein kinase 8
, LOW QUALITY PROTEIN: mitogen-activated protein kinase 8B-like
, MAP kinase 8B
, MAPK 8B
, Mitogen-activated protein kinase 8B
, Stress-activated protein kinase JNKb
, c-Jun N-terminal kinase B