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anti-Human JNK Antibodies:
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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
Show all 11 Pubmed References
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
Show all 7 Pubmed References
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
Show all 5 Pubmed References
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
Show all 4 Pubmed References
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
Show all 4 Pubmed References
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
Show all 3 Pubmed References
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
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
Show all 6 Pubmed References
Here we uncover a cell non-autonomous requirement for the Epidermal growth factor receptor (Egfr (show EGFR Antibodies)) pathway in the lateral epidermis for sustained dpp (show TGFb Antibodies) expression in the LE. Specifically, we demonstrate that Egfr (show EGFR Antibodies) 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 (show SCRIB Antibodies)) tumors requires bZIP protein Fos, the ETS (show ETS1 Antibodies)-domain factor Ets21c and the nuclear receptor Ftz-F1 (show NR5A2 Antibodies), all acting downstream of Jun-N-terminal kinase.
Diminished MTORC1-dependent JNK activation underlies the neurodevelopmental defects associated with lysosomal dysfunction.
ROS (show ROS1 Antibodies)/JNK/p38 (show MAPK14 Antibodies)/Upd (show UROD Antibodies) 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 (show NOTCH1 Antibodies)-Src (show SRC Antibodies) synergy.
This study demonstrated that the mechanism by which Bsk (show FRK Antibodies) is required for pruning is through reducing the membrane levels of the adhesion molecule (show NCAM1 Antibodies) Fasciclin II (show NCAM2 Antibodies) (FasII)
Study solves the crystal structure of unphosphorylated DJNK in complex with adenylyl imidodiphosphate (AMP (show AMPH Antibodies)-PNP (show NP Antibodies)) 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 (show TARDBP Antibodies)-associated neurodegeneration and the balance between cytoprotective JNK and cytotoxic p38 (show MAPK14 Antibodies) signaling dictates phenotypic outcome to TDP-43 (show TARDBP Antibodies) 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 (show FOSB Antibodies), and CHOP (show DDIT3 Antibodies) may interfere with complete autophagy.
The findings indicate that ERK (show EPHB2 Antibodies) and JNK signaling pathways, as well as NF-kappaB (show NFKB1 Antibodies)-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 (show G3BP1 Antibodies) 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 (show NOTCH1 Antibodies) signaling via activation of c-Jun (show JUN Antibodies) and indicate that JNK/c-Jun/Notch1 (show NOTCH1 Antibodies) signaling is a potential therapeutic target for TNBC
Here, the authors show that the CDK (show CDK4 Antibodies) inhibitor p21 (CDKN1A (show CDKN1A Antibodies)) maintains the viability of DNA damage-induced senescent cells. Upon p21 (show CDKN1A Antibodies) knockdown, senescent cells acquired multiple DNA lesions that activated ataxia telangiectasia mutated (ATM (show ATM Antibodies)) and nuclear factor (NF)-kappaB (show NFKB1 Antibodies) kinase, leading to decreased cell survival. NF-kappaB (show NFKB1 Antibodies) activation induced TNF-alpha (show TNF Antibodies) secretion and JNK activation to mediate death of senescent cells in a...
Results indicate that cordycepin promotes caveolin-1 (CAV1 (show CAV1 Antibodies))upregulation to enhance c-jun N-terminal kinase (JNK)/forkhead box O3A (show FOXO3 Antibodies) protein (Foxo3a (show FOXO3 Antibodies)) 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 (show MCL1 Antibodies)) expression and c-Jun N-terminal kinase 1 (JNK1) activation and subsequent Bcl-xL (show BCL2L1 Antibodies) protein degradation.
identified the c-Jun N-terminal kinase 1 (JNK1) as the kinase involved in the phosphorylation of NEIL1 (show NEIL1 Antibodies)
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 (show MAPK1 Antibodies) pathway in diabetes mellitus.
The increase in c-Jun N-terminal kinase (c-Jun) and specificity protein 1 (SP1 (show SP1 Antibodies)) expressions was positively correlated with transforming growth factor beta 1 (TGFbeta1 (show TGFB1 Antibodies)) in both high glucose-treated renal mesangial cells (HRMCs) and diabetic kidneys.
JNK1-mediated NLRP3 (show NLRP3 Antibodies) phosphorylation at S194 is a critical priming event and is essential for NLRP3 (show NLRP3 Antibodies) inflammasome activation.
The purpose of this study was to investigate mechanisms that govern the regulation of Npnt (show NPNT Antibodies) gene expression by IL-1beta (show IL1B Antibodies) in osteoblasts.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (show ROS1 Antibodies)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (show TP53 Antibodies), p38 (show CRK Antibodies) and JNK MAPKs, culminating in an increase in autophagy and apoptosis markers.
IL-6 (show IL6 Antibodies) likely up-regulates IRP1 (show ACO1 Antibodies) and DMT1 (show SLC11A2 Antibodies) expression and down-regulates FPN1 (show SLC40A1 Antibodies) expression in BV2 (show DNAH9 Antibodies) 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 (show VTI1B Antibodies) proteins; data suggest that JNK-dependent phosphorylation of T-SNARE (show VTI1B Antibodies) proteins may have an important functional role in synaptic plasticity.
JNK signaling, which is inversely correlated with WNT4 (show WNT4 Antibodies), plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin (show CDH1 Antibodies) 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 (show XBP1 Antibodies).
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 (show CASP3 Antibodies)-dependent Proteolysis of JNK1-2 and Bid (show BID Antibodies).
JNK signaling is required to establish microtubule stability and maintain tissue cohesion in the gut (show GUSB Antibodies).
Data show that the death pathway is independent of ERK (show MAPK1 Antibodies) but relies on activating Bad phosphorylation through the control of both kinases Cdk1 (show CDK1 Antibodies) and JNK.
study reports MPK8 connects protein phosphorylation, Ca(2 (show CA2 Antibodies))+ and ROS (show ROS1 Antibodies) in wound-signaling pathway; suggests 2 major activation modes, Ca(2 (show CA2 Antibodies))+/CaMs and MAP kinase (show MAPK1 Antibodies) phosphorylation cascade, converge at MPK8 to monitor or maintain an essential part of ROS (show ROS1 Antibodies) homeostasis
our data provide strong evidence that Jip3 in fact serves as an adapter protein linking these cargos to dynein
P38 (show MAPK14 Antibodies) and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
A dorsalization pathway that is exerted by Axin (show AXIN1 Antibodies)/JNK signaling and its inhibitor Aida (show AIDA Antibodies) during vertebrate embryogenesis, is defined.
JNK-Mmp13 (show MMP13 Antibodies) 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 (show INS Antibodies)-IGF-1 (show IGF1 Antibodies) 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 (show MAPK1 Antibodies) (MAPK (show MAPK1 Antibodies)) signaling pathway, which is regulated by MLK-1 (show MAP3K9 Antibodies) MAPK (show MAPK1 Antibodies) kinase kinase (MAPKKK), MEK-1 (show MAP2K1 Antibodies) MAPK (show MAPK1 Antibodies) kinase (MAPKK), and KGB-1 (show KCNJ3 Antibodies) JNK-like MAPK (show MAPK1 Antibodies).
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