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Cow (Bovine) Polyclonal JNK Primary Antibody for IF (p), IHC (p) - ABIN732368
Rosenzweig, Djap, Ou, Quinn: Mechanical injury of bovine cartilage explants induces depth-dependent, transient changes in MAP kinase activity associated with apoptosis. in Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society 2012
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Human Monoclonal JNK Primary Antibody for IP, WB - ABIN967330
Adler, Fuchs, Kim, Kraft, King, Pelling, Ronai: jun-NH2-terminal kinase activation mediated by UV-induced DNA lesions in melanoma and fibroblast cells. in Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1996
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Human Monoclonal JNK Primary Antibody for FACS, WB - ABIN968867
Fleming, Armstrong, Morrice, Paterson, Goedert, Cohen: Synergistic activation of stress-activated protein kinase 1/c-Jun N-terminal kinase (SAPK1/JNK) isoforms by mitogen-activated protein kinase kinase 4 (MKK4) and MKK7. in The Biochemical journal 2001
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Human Monoclonal JNK Primary Antibody for ICS - ABIN1177076
Huang, Shi, Chi: Regulation of JNK and p38 MAPK in the immune system: signal integration, propagation and termination. in Cytokine 2009
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Human Monoclonal JNK Primary Antibody for FACS, WB - ABIN968866
Kyriakis, Avruch: Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation. in Physiological reviews 2001
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Human Monoclonal JNK Primary Antibody for ICS - ABIN1177075
Wagner, Nebreda: Signal integration by JNK and p38 MAPK pathways in cancer development. in Nature reviews. Cancer 2009
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Human Polyclonal JNK Primary Antibody for IHC, IHC (p) - ABIN4327961
Gao, Wang, Zhang, Yu, Ji, Wang, Zhang, Jiang, Jin, Huang, Zhang, Li: Tumor necrosis factor receptor-associated factor 5 (Traf5) acts as an essential negative regulator of hepatic steatosis. in Journal of hepatology 2016
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Caenorhabditis elegans (C. elegans) Polyclonal JNK Primary Antibody for IHC (p), IHC - ABIN151424
Oh, Mukhopadhyay, Svrzikapa, Jiang, Davis, Tissenbaum: JNK regulates lifespan in Caenorhabditis elegans by modulating nuclear translocation of forkhead transcription factor/DAF-16. in Proceedings of the National Academy of Sciences of the United States of America 2005
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Human Polyclonal JNK Primary Antibody for WB - ABIN3043004
Zheng, Liu, Liu, Ma, Zhou, Chen, Chang, Wang, Yang, He: Cucurbitacin B inhibits growth and induces apoptosis through the JAK2/STAT3 and MAPK pathways in SH?SY5Y human neuroblastoma cells. in Molecular medicine reports 2014
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Human Polyclonal JNK Primary Antibody for IF, IHC (p) - ABIN391724
Deng, Ren, Yang, Lin, Wu: A JNK-dependent pathway is required for TNFalpha-induced apoptosis. in Cell 2003
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Data show that JNK signalling inhibits the growth of losers, while JAK (显示 JAK3 抗体)/STAT (显示 STAT1 抗体) signalling promotes competition-induced winner cell proliferation.
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr (显示 EGFR 抗体)) pathway in the lateral epidermis for sustained dpp (显示 TGFb 抗体) expression in the LE. Specifically, we demonstrate that Egfr (显示 EGFR 抗体) 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 (显示 SCRIB 抗体)) tumors requires bZIP protein Fos, the ETS (显示 ETS1 抗体)-domain factor Ets21c and the nuclear receptor Ftz-F1 (显示 NR5A2 抗体), all acting downstream of Jun-N-terminal kinase.
Diminished MTORC1-dependent JNK activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (显示 ROS1 抗体)/JNK/p38 (显示 MAPK14 抗体)/Upd (显示 UROD 抗体) 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 (显示 NOTCH1 抗体)-Src (显示 SRC 抗体) synergy.
This study demonstrated that the mechanism by which Bsk (显示 FRK 抗体) is required for pruning is through reducing the membrane levels of the adhesion molecule (显示 NCAM1 抗体) Fasciclin II (显示 NCAM2 抗体) (FasII)
Study solves the crystal structure of unphosphorylated DJNK in complex with adenylyl imidodiphosphate (AMP (显示 AMPH 抗体)-PNP (显示 NP 抗体)) and magnesium.
PERK/ATF4 activated the JNK pathway through Rac1 and Slpr activation in apoptotic cells.
PRDM5 (显示 PRDM5 抗体) promotes the proliferation and invasion of murine melanoma cells through up-regulating JNK expression and strategies targeting PRDM5 (显示 PRDM5 抗体) may be promising for the therapy of melanoma.
This study showed that the induction level of IL-32 (显示 IL32 抗体) was increased in chronic rhinosinusitis with nasal polyps compared to normal nasal mucosa and that LPS (显示 IRF6 抗体)-induced IL-32 (显示 IL32 抗体) expression in nasal polyp-derived fibroblasts was regulated via the TLR4 (显示 TLR4 抗体)/JNK/AKT (显示 AKT1 抗体)/CREB (显示 CREB1 抗体) signaling pathway.
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK, AP-1 (显示 FOSB 抗体), and CHOP (显示 DDIT3 抗体) may interfere with complete autophagy.
The findings indicate that ERK (显示 EPHB2 抗体) and JNK signaling pathways, as well as NF-kappaB (显示 NFKB1 抗体)-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 (显示 G3BP1 抗体) 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 (显示 NOTCH1 抗体) signaling via activation of c-Jun (显示 JUN 抗体) and indicate that JNK/c-Jun/Notch1 (显示 NOTCH1 抗体) signaling is a potential therapeutic target for TNBC
Here, the authors show that the CDK (显示 CDK4 抗体) inhibitor p21 (CDKN1A (显示 CDKN1A 抗体)) maintains the viability of DNA damage-induced senescent cells. Upon p21 (显示 CDKN1A 抗体) knockdown, senescent cells acquired multiple DNA lesions that activated ataxia telangiectasia mutated (ATM (显示 ATM 抗体)) and nuclear factor (NF)-kappaB (显示 NFKB1 抗体) kinase, leading to decreased cell survival. NF-kappaB (显示 NFKB1 抗体) activation induced TNF-alpha (显示 TNF 抗体) secretion and JNK activation to mediate death of senescent cells in a...
Results indicate that cordycepin promotes caveolin-1 (CAV1 (显示 CAV1 抗体))upregulation to enhance c-jun N-terminal kinase (JNK)/forkhead box O3A (显示 FOXO3 抗体) protein (Foxo3a (显示 FOXO3 抗体)) 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 (显示 MCL1 抗体)) expression and c-Jun N-terminal kinase 1 (JNK1) activation and subsequent Bcl-xL (显示 BCL2L1 抗体) protein degradation.
identified the c-Jun N-terminal kinase 1 (JNK1) as the kinase involved in the phosphorylation of NEIL1 (显示 NEIL1 抗体)
The authors have found that JNK signaling is required for proper vascular morphogenesis and the normal formation of collateral arteries in muscle.
JNK1-mediated NLRP3 (显示 NLRP3 抗体) phosphorylation at S194 is a critical priming event and is essential for NLRP3 (显示 NLRP3 抗体) inflammasome activation.
The purpose of this study was to investigate mechanisms that govern the regulation of Npnt (显示 NPNT 抗体) gene expression by IL-1beta (显示 IL1B 抗体) in osteoblasts.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (显示 ROS1 抗体)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (显示 TP53 抗体), p38 (显示 CRK 抗体) and JNK MAPKs, culminating in an increase in autophagy and apoptosis markers.
IL-6 (显示 IL6 抗体) likely up-regulates IRP1 (显示 ACO1 抗体) and DMT1 (显示 SLC11A2 抗体) expression and down-regulates FPN1 (显示 SLC40A1 抗体) expression in BV2 (显示 DNAH9 抗体) 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 (显示 VTI1B 抗体) proteins; data suggest that JNK-dependent phosphorylation of T-SNARE (显示 VTI1B 抗体) proteins may have an important functional role in synaptic plasticity.
JNK signaling, which is inversely correlated with WNT4 (显示 WNT4 抗体), plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin (显示 CDH1 抗体) 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 (显示 XBP1 抗体).
Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3 (显示 CASP3 抗体)-dependent Proteolysis of JNK1-2 and Bid (显示 BID 抗体).
JNK signaling is required to establish microtubule stability and maintain tissue cohesion in the gut (显示 GUSB 抗体).
Data show that the death pathway is independent of ERK (显示 MAPK1 抗体) but relies on activating Bad phosphorylation through the control of both kinases Cdk1 (显示 CDK1 抗体) and JNK.
study reports MPK8 connects protein phosphorylation, Ca(2 (显示 CA2 抗体))+ and ROS (显示 ROS1 抗体) in wound-signaling pathway; suggests 2 major activation modes, Ca(2 (显示 CA2 抗体))+/CaMs and MAP kinase (显示 MAPK1 抗体) phosphorylation cascade, converge at MPK8 to monitor or maintain an essential part of ROS (显示 ROS1 抗体) homeostasis
our data provide strong evidence that Jip3 in fact serves as an adapter protein linking these cargos to dynein
P38 (显示 MAPK14 抗体) and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
A dorsalization pathway that is exerted by Axin (显示 AXIN1 抗体)/JNK signaling and its inhibitor Aida (显示 AIDA 抗体) during vertebrate embryogenesis, is defined.
JNK-Mmp13 (显示 MMP13 抗体) 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 (显示 INS 抗体)-IGF-1 (显示 IGF1 抗体) 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 (显示 MAPK1 抗体) (MAPK (显示 MAPK1 抗体)) signaling pathway, which is regulated by MLK-1 (显示 MAP3K9 抗体) MAPK (显示 MAPK1 抗体) kinase kinase (MAPKKK), MEK-1 (显示 MAP2K1 抗体) MAPK (显示 MAPK1 抗体) kinase (MAPKK), and KGB-1 (显示 KCNJ3 抗体) JNK-like MAPK (显示 MAPK1 抗体).
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