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Noguchi, Naziruddin, Shimoda, Fujita, Chujo, Takita, Peng, Sugimoto, Itoh, Tamura, Olsen, Kobayashi, Onaca, Levy, Matsumoto: Comparison of fresh and cultured islets from human and porcine pancreata. dans Transplantation proceedings 2010
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Human JNK Kit ELISA pour Cell ELISA - ABIN1981833
Hinton, Henderson, Blanks, Rudnicka, Miller: Monoclonal antibodies react with neuronal subpopulations in the human nervous system. dans The Journal of comparative neurology 1988
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Shintani, Hollingsworth, Wheelock, Johnson: Collagen I promotes metastasis in pancreatic cancer by activating c-Jun NH(2)-terminal kinase 1 and up-regulating N-cadherin expression. dans Cancer research 2006
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Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr (Montrer EGFR Kits ELISA)) pathway in the lateral epidermis for sustained dpp (Montrer TGFb Kits ELISA) expression in the LE. Specifically, we demonstrate that Egfr (Montrer EGFR Kits ELISA) 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 Kits ELISA)) tumors requires bZIP protein Fos, the ETS (Montrer ETS1 Kits ELISA)-domain factor Ets21c and the nuclear receptor Ftz-F1 (Montrer NR5A2 Kits ELISA), all acting downstream of Jun-N-terminal kinase.
Diminished MTORC1-dependent JNK activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (Montrer ROS1 Kits ELISA)/JNK/p38 (Montrer MAPK14 Kits ELISA)/Upd (Montrer UROD Kits ELISA) 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 Kits ELISA)-Src (Montrer SRC Kits ELISA) synergy.
This study demonstrated that the mechanism by which Bsk (Montrer FRK Kits ELISA) is required for pruning is through reducing the membrane levels of the adhesion molecule (Montrer NCAM1 Kits ELISA) Fasciclin II (Montrer NCAM2 Kits ELISA) (FasII)
Study solves the crystal structure of unphosphorylated DJNK in complex with adenylyl imidodiphosphate (AMP (Montrer AMPH Kits ELISA)-PNP (Montrer NP Kits ELISA)) 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 (Montrer TARDBP Kits ELISA)-associated neurodegeneration and the balance between cytoprotective JNK and cytotoxic p38 (Montrer MAPK14 Kits ELISA) signaling dictates phenotypic outcome to TDP-43 (Montrer TARDBP Kits ELISA) expression in Drosophila.
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK, AP-1 (Montrer FOSB Kits ELISA), and CHOP (Montrer DDIT3 Kits ELISA) may interfere with complete autophagy.
The findings indicate that ERK (Montrer EPHB2 Kits ELISA) and JNK signaling pathways, as well as NF-kappaB (Montrer NFKB1 Kits ELISA)-mediated signaling are important contributors to the pathogenesis of Kashin-Beck disease.
The data suggested that JNK-enhanced Tudor-SN phosphorylation promotes the interaction between Tudor-SN and G3BP (Montrer G3BP1 Kits ELISA) and facilitates the efficient recruitment of Tudor-SN into stress granules under conditions of sodium arsenite-induced oxidative stress.
Taken together, our data demonstrate that JNK regulates triple-negative breast cancer (TNBC)tumorigenesis by promoting CSC phenotype through Notch1 (Montrer NOTCH1 Kits ELISA) signaling via activation of c-Jun (Montrer JUN Kits ELISA) and indicate that JNK/c-Jun/Notch1 (Montrer NOTCH1 Kits ELISA) signaling is a potential therapeutic target for TNBC
Here, the authors show that the CDK (Montrer CDK4 Kits ELISA) inhibitor p21 (CDKN1A (Montrer CDKN1A Kits ELISA)) maintains the viability of DNA damage-induced senescent cells. Upon p21 (Montrer CDKN1A Kits ELISA) knockdown, senescent cells acquired multiple DNA lesions that activated ataxia telangiectasia mutated (ATM (Montrer ATM Kits ELISA)) and nuclear factor (NF)-kappaB (Montrer NFKB1 Kits ELISA) kinase, leading to decreased cell survival. NF-kappaB (Montrer NFKB1 Kits ELISA) activation induced TNF-alpha (Montrer TNF Kits ELISA) secretion and JNK activation to mediate death of senescent cells in a...
Results indicate that cordycepin promotes caveolin-1 (CAV1 (Montrer CAV1 Kits ELISA))upregulation to enhance c-jun N-terminal kinase (JNK)/forkhead box O3A (Montrer FOXO3 Kits ELISA) protein (Foxo3a (Montrer FOXO3 Kits ELISA)) signaling pathway activation, inducing apoptosis in lung cancer cells.
The combination of 2-deoxyglucose (2-DG) and ABT-199 initiated cell death through the reduction of myeloid cell leukemia sequence 1 protein (Mcl-1 (Montrer MCL1 Kits ELISA)) expression and c-Jun N-terminal kinase 1 (JNK1) activation and subsequent Bcl-xL (Montrer BCL2L1 Kits ELISA) protein degradation.
identified the c-Jun N-terminal kinase 1 (JNK1) as the kinase involved in the phosphorylation of NEIL1 (Montrer NEIL1 Kits ELISA)
This study suggests that advanced glycation end products (AGEs) and activation of AGEs receptor could induce the proliferation of smooth muscle cells from Saphenous vein but not smooth muscle cells from internal thoracic arteryvia MAP kinase (Montrer MAPK1 Kits ELISA) pathway in diabetes mellitus.
The increase in c-Jun N-terminal kinase (c-Jun) and specificity protein 1 (SP1 (Montrer SP1 Kits ELISA)) expressions was positively correlated with transforming growth factor beta 1 (TGFbeta1 (Montrer TGFB1 Kits ELISA)) in both high glucose-treated renal mesangial cells (HRMCs) and diabetic kidneys.
JNK1-mediated NLRP3 (Montrer NLRP3 Kits ELISA) phosphorylation at S194 is a critical priming event and is essential for NLRP3 (Montrer NLRP3 Kits ELISA) inflammasome activation.
The purpose of this study was to investigate mechanisms that govern the regulation of Npnt (Montrer NPNT Kits ELISA) gene expression by IL-1beta (Montrer IL1B Kits ELISA) in osteoblasts.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (Montrer ROS1 Kits ELISA)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (Montrer TP53 Kits ELISA), p38 (Montrer CRK Kits ELISA) and JNK MAPKs, culminating in an increase in autophagy and apoptosis markers.
IL-6 (Montrer IL6 Kits ELISA) likely up-regulates IRP1 (Montrer ACO1 Kits ELISA) and DMT1 (Montrer SLC11A2 Kits ELISA) expression and down-regulates FPN1 (Montrer SLC40A1 Kits ELISA) expression in BV2 (Montrer DNAH9 Kits ELISA) microglial cells through JNK signaling pathways
Study examined whether JNK is present at the presynaptic site and its activity after presynaptic NMDA receptors stimulation; found that JNK, via the JBD domain, acts as a physiological effector on T-SNARE (Montrer VTI1B Kits ELISA) proteins; data suggest that JNK-dependent phosphorylation of T-SNARE (Montrer VTI1B Kits ELISA) proteins may have an important functional role in synaptic plasticity.
JNK signaling, which is inversely correlated with WNT4 (Montrer WNT4 Kits ELISA), plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin (Montrer CDH1 Kits ELISA) junctions between oocytes in mouse ovaries.
It was concluded that compounds targeting JNK1 activity in brain and adipose tissue, which do not accumulate in the skin, may be safer and most effective.
JNK1 activation suppresses antifungal immunity in mice. JNK1-deficient mice had a significantly higher survival rate than wild-type control mice in response to Candida albicans infection, and the expression of JNK1 in hematopoietic innate immune cells was critical for this effect.
activation of JNK in the endoplasmic reticulum stress response precedes activation of XBP1 (Montrer XBP1 Kits ELISA).
Data suggest that single muscle immobilization induces a shift of myosin heavy chain (MHC) isoforms composition toward a faster contractile phenotype and decreases the polymorphic profile of single fibres, and that activation of p38 and JNK could be a potential mechanism involved in these contractile phenotype modifications during muscle immobilization.
Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3 (Montrer CASP3 Kits ELISA)-dependent Proteolysis of JNK1-2 and Bid (Montrer BID Kits ELISA).
JNK signaling is required to establish microtubule stability and maintain tissue cohesion in the gut (Montrer GUSB Kits ELISA).
Data show that the death pathway is independent of ERK (Montrer MAPK1 Kits ELISA) but relies on activating Bad phosphorylation through the control of both kinases Cdk1 (Montrer CDK1 Kits ELISA) and JNK.
study reports MPK8 connects protein phosphorylation, Ca(2 (Montrer CA2 Kits ELISA))+ and ROS (Montrer ROS1 Kits ELISA) in wound-signaling pathway; suggests 2 major activation modes, Ca(2 (Montrer CA2 Kits ELISA))+/CaMs and MAP kinase (Montrer MAPK1 Kits ELISA) phosphorylation cascade, converge at MPK8 to monitor or maintain an essential part of ROS (Montrer ROS1 Kits ELISA) homeostasis
our data provide strong evidence that Jip3 in fact serves as an adapter protein linking these cargos to dynein
P38 (Montrer MAPK14 Kits ELISA) and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
A dorsalization pathway that is exerted by Axin (Montrer AXIN1 Kits ELISA)/JNK signaling and its inhibitor Aida (Montrer AIDA Kits ELISA) during vertebrate embryogenesis, is defined.
JNK-Mmp13 (Montrer MMP13 Kits ELISA) signaling pathway plays an essential role in regulating the innate immune cell migration in response to severe injury in vivo
Our genetic study unravelled the underlying pathway where JNK-1 is acting independently of insulin (Montrer INS Kits ELISA)-IGF-1 (Montrer IGF1 Kits ELISA) 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 Kits ELISA) (MAPK (Montrer MAPK1 Kits ELISA)) signaling pathway, which is regulated by MLK-1 MAPK (Montrer MAPK1 Kits ELISA) kinase kinase (MAPKKK), MEK-1 (Montrer MAP2K1 Kits ELISA) MAPK (Montrer MAPK1 Kits ELISA) kinase (MAPKK), and KGB-1 (Montrer KCNJ3 Kits ELISA) JNK-like MAPK (Montrer MAPK1 Kits ELISA).
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 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
, 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
, mitogen-activated protein kinase 8