Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
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
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
CXCL12 (Montrer CXCL12 Protéines) activates the MEKK1 (Montrer MAP3K1 Protéines)/JNK signaling pathway, which in turn initiates SMAD3 (Montrer SMAD3 Protéines) phosphorylation, its translocation to nuclei, and recruitment of SMAD3 (Montrer SMAD3 Protéines) to the CTGF (Montrer CTGF Protéines) promoter, which ultimately induces CTGF (Montrer CTGF Protéines) 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 (Montrer JUN Protéines).
Inhibition of each TGFbeta (Montrer TGFB1 Protéines) receptor-I, glucocorticoid receptor (Montrer NR3C1 Protéines) 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 (Montrer NR3C1 Protéines)
JNK inhibitor prevents SIRT1 (Montrer SIRT1 Protéines) phosphorylation, leading to elevated SIRT1 (Montrer SIRT1 Protéines) 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 (Montrer SIRT1 Protéines).
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 (Montrer ANXA2 Protéines) induces cisplatin resistance of non-small cell lung cancer (NSCLC)via regulation of JNK/c-Jun/p53 (Montrer TP53 Protéines) signaling, and provided an evidence that blockade of Annexin A2 (Montrer ANXA2 Protéines) 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 (Montrer ROS1 Protéines)-JNK-p53 (Montrer TP53 Protéines) 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.
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 (Montrer INS Protéines)-IGF-1 (Montrer IGF1 Protéines) 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 (Montrer MAPK1 Protéines) (MAPK (Montrer MAPK1 Protéines)) signaling pathway, which is regulated by MLK-1 (Montrer MAP3K9 Protéines) MAPK (Montrer MAPK1 Protéines) kinase kinase (MAPKKK), MEK-1 (Montrer MAP2K1 Protéines) MAPK (Montrer MAPK1 Protéines) kinase (MAPKK), and KGB-1 (Montrer KCNJ3 Protéines) JNK-like MAPK (Montrer MAPK1 Protéines).
High JNK expression is associated with cerebral ischaemia reperfusion injury.
Noise exposure led to enhanced JNK phosphorylation and IRS1 (Montrer IRS1 Protéines) serine phosphorylation as well as reduced Akt (Montrer AKT1 Protéines) phosphorylation in skeletal muscles in response to exogenous insulin (Montrer INS Protéines) stimulation.
Prdx1 (Montrer PRDX1 Protéines) knockout can aggravate the oxidative stress and lung injury by increasing the level of Reactive Oxygen Species (ROS (Montrer ROS1 Protéines)), and also activate P38 (Montrer CRK Protéines)/JNK signaling pathway.
Data identify a unique signal crosstalk between Wnt (Montrer WNT2 Protéines) signaling and the MAP3K1 (Montrer MAP3K1 Protéines)-JNK pathway in epithelial morphogenesis.
Therefore, APP (Montrer APP Protéines) modulates Nav1.6 (Montrer SCN8A Protéines) sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP (Montrer APP Protéines) at Thr668.
These interactions are required for SRC (Montrer SRC Protéines)-induced activation of VAV (Montrer VAV1 Protéines) and the subsequent engagement of a JIP1 (Montrer MAPK8IP1 Protéines)-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 (Montrer CRK Protéines) 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.
Cell fusion during wound healing in Drosophila larval epidermis occurred primarily in the wound vicinity, where JAK (Montrer JAK3 Protéines)/STAT (Montrer STAT1 Protéines) activation was suppressed by fusion-inducing JNK signaling.
aken together, these results reveal that inactivation of Rpd3 (Montrer HDAC1 Protéines) independently regulates JNK and Yki (Montrer YAP1 Protéines) activities and that both Hippo and JNK signaling pathways contribute to Rpd3 (Montrer HDAC1 Protéines) RNAi-induced apoptosis.
Data show that JNK signalling inhibits the growth of losers, while JAK (Montrer JAK3 Protéines)/STAT (Montrer STAT1 Protéines) signalling promotes competition-induced winner cell proliferation.
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr (Montrer EGFR Protéines)) pathway in the lateral epidermis for sustained dpp (Montrer TGFb Protéines) expression in the LE. Specifically, we demonstrate that Egfr (Montrer EGFR Protéines) 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 (Montrer SCRIB Protéines)) tumors requires bZIP protein Fos, the ETS (Montrer ETS1 Protéines)-domain factor Ets21c and the nuclear receptor Ftz-F1 (Montrer NR5A2 Protéines), all acting downstream of Jun-N-terminal kinase.
Diminished MTORC1-dependent JNK activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (Montrer ROS1 Protéines)/JNK/p38 (Montrer MAPK14 Protéines)/Upd (Montrer UROD Protéines) 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 (Montrer NOTCH1 Protéines)-Src (Montrer SRC Protéines) synergy.
This study demonstrated that the mechanism by which Bsk (Montrer FRK Protéines) is required for pruning is through reducing the membrane levels of the adhesion molecule (Montrer NCAM1 Protéines) Fasciclin II (Montrer NCAM2 Protéines) (FasII)
Porcine reproductive and respiratory syndrome virus -activated TAK-1 (Montrer NR2C2 Protéines) was essential for the activation of JNK and NF-kappaB (Montrer NFKB1 Protéines) pathways and IL-8 (Montrer IL8 Protéines) expression.
Data show that proinflammatory cytokines induction was ERK1/2 and JNK1/2 dependent.
These data suggest that the p38 (Montrer MAPK14 Protéines) 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 (Montrer MAPK14 Protéines) 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 (Montrer PPP2R2B Protéines) and AIP1 (Montrer PDCD6IP Protéines) cooperatively induce activation of ASK1 (Montrer MAP3K5 Protéines)-JNK signaling and vascular endothelial cell apoptosis.
Phorbol 12-myristate 13-acetate activation of ERK (Montrer MAPK1 Protéines) 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 (Montrer CA2 Protéines))+ and ROS (Montrer ROS1 Protéines) in wound-signaling pathway; suggests 2 major activation modes, Ca(2 (Montrer CA2 Protéines))+/CaMs and MAP kinase (Montrer MAPK1 Protéines) phosphorylation cascade, converge at MPK8 to monitor or maintain an essential part of ROS (Montrer ROS1 Protéines) 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 (Montrer CASP3 Protéines)-dependent Proteolysis of JNK1-2 and Bid (Montrer BID Protéines).
JNK signaling is required to establish microtubule stability and maintain tissue cohesion in the gut (Montrer GUSB Protéines).
Data show that the death pathway is independent of ERK (Montrer MAPK1 Protéines) but relies on activating Bad phosphorylation through the control of both kinases Cdk1 (Montrer CDK1 Protéines) and JNK.
our data provide strong evidence that Jip3 in fact serves as an adapter protein linking these cargos to dynein
P38 (Montrer MAPK14 Protéines) and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
A dorsalization pathway that is exerted by Axin (Montrer AXIN1 Protéines)/JNK signaling and its inhibitor Aida (Montrer AIDA Protéines) during vertebrate embryogenesis, is defined.
JNK-Mmp13 (Montrer MMP13 Protéines) 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 (Montrer MAPK14 Protéines) in TNF (Montrer TNF Protéines) regulation of E2F1 (Montrer E2F1 Protéines). Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (Montrer TNF Protéines)-mediated EC dysfunction.
PKD (Montrer PRKD1 Protéines) is a critical mediator in H2O2- but not TNF (Montrer TNF Protéines)-induced ASK1 (Montrer MAP3K5 Protéines)-JNK signaling
ATF3 (Montrer ATF3 Protéines) 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 (Montrer IRF6 Protéines)
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