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Human Polyclonal MAPK9 Primary Antibody for IHC (p), WB - ABIN1882172
Gupta, Barrett, Whitmarsh, Cavanagh, Sluss, Dérijard, Davis: Selective interaction of JNK protein kinase isoforms with transcription factors. in The EMBO journal 1996
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Human Polyclonal MAPK9 Primary Antibody for ELISA, WB - ABIN4327970
Leppä, Bohmann: Diverse functions of JNK signaling and c-Jun in stress response and apoptosis. in Oncogene 1999
RhoGDIbeta overexpression led to downregulation of miR (show MLXIP Antibodies)-200c, whereas miR (show MLXIP Antibodies)-200c was able directly to target 3'-UTR (show UTS2R Antibodies) of jnk2mRNA and attenuated JNK2 protein translation, which resulted in attenuation of Sp1mRNA and protein expression in turn, inhibiting Sp1 (show PSG1 Antibodies)-dependent MMP-2 (show MMP2 Antibodies) transcription.
The MAP kinase (show MAPK1 Antibodies) JNK2 mediates cigarette smoke-induced tissue factor (show F3 Antibodies) activation, arterial thrombosis and reactive oxygen species production.
We found p-JNK2 up-regulation in AUC and its early down-regulation in UC-CRC (show CALR Antibodies) and CRC (show CALR Antibodies) carcinogenesis.
JNK2 was a novel direct target of miR (show MLXIP Antibodies)-20a-5p.
The release of infectious respiratory syncytial virus (RSV) virions from infected cells was significantly reduced by JNK1 (show MAPK8 Antibodies)/2 siRNA knockdown, implicating JNK1 (show MAPK8 Antibodies)/2 as a key host factor for RSV virus production.
PXR (show NR1I2 Antibodies) regulates the intestinal epithelial barrier during inflammation by modulating cytokine-induced MLCK (show MYLK Antibodies) expression and JNK1 (show MAPK8 Antibodies)/2 activation
Phloretin is able to inhibit NSCLC A549 cell growth by inducing apoptosis through P38 MAPK (show MAPK14 Antibodies) and JNK1 (show MAPK8 Antibodies)/2 pathways, and therefore may prove to be an adjuvant to the treatment of non-small cell lung cancer
In hepatocytes, JNK1 (show MAPK8 Antibodies) and JNK2 appear to have combined effects in protecting from drug-induced liver injury.
Inhibition of JNK1 (show MAPK8 Antibodies)/2 activity suppressed Hedgehog (show SHH Antibodies) pathway activity in acquired chemoresistant cancer cells.
although JNK (show MAPK8 Antibodies) activation and RIP3 (show RIPK3 Antibodies) expression are induced by FS, neither contributes to the liver injury.
these results identify a protective role of epithelial JNK2 signaling to maintain mucosal barrier function, epithelial cell integrity, and mucus layer production in the event of inflammatory tissue damage
activation of JNK (show MAPK8 Antibodies) in the endoplasmic reticulum stress response precedes activation of XBP1 (show XBP1 Antibodies).
JNK-2 regulates aggrecan (show ACAN Antibodies) degradation in cultured murine cartilage and surgically induced osteoarthritis in vivo following mechanical destabilization of the knee joint.
activation of astrocyte MMP2 (show MMP2 Antibodies)/JNK1 (show MAPK8 Antibodies)/2 contributes to the pathogenesis of pain hypersensitivity in the complex regional pain syndrome model
JNK1 (show MAPK8 Antibodies)/2-dependent regulation of p66ShcS36 phosphorylation, is reported.
This study demonstrated that the disruption of JNK2 appears to have a greater impact on tolerance than the other isoforms in the tail-flick but not the hot-plate test.
although JNK (show MAPK8 Antibodies) activation and RIP3 (show MPRIP Antibodies) expression are induced by FS, neither contributes to the liver injury.
morphine activated JNK2 through an arrestin-independent Src- and PKC-dependent mechanism, whereas fentanyl activated JNK2 through a Src-GRK3/arrestin-2-dependent and PKC-independent mechanism.
this study indicates that JNK2 is a physiological kinase responsible for eNOS (show NOS3 Antibodies)-Ser (show SIGLEC1 Antibodies)(116) phosphorylation and regulates NO production.
Data show that proinflammatory cytokines induction was ERK1/2 and JNK1 (show MAPK8 Antibodies)/2 dependent.
These data suggest that the p38 (show MAPK14 Antibodies) and JNK (show MAPK8 Antibodies) signaling pathways play pivotal roles in PRRSV replication and may regulate immune responses during virus infection.
MPK9 and MPK12 (show MAPK12 Antibodies) are positive regulators of salicylic acid signaling in Arabidopsis guard cells.
MPK9 and MPK12 (show MAPK12 Antibodies) are key regulators mediating both abscisic acid (ABA) and Methyl jasmonate (MeJA) signalling in guard cells.
Data suggest that MPK9 is autoactivated via phosphorylation independent of any upstream MAPK (show MAPK1 Antibodies) kinase signaling; autophosphorylation occurs at both threonine and tyrosine residues in Thr (show TRH Antibodies)-Asp (show ASIP Antibodies)-Tyr (show TYR Antibodies) motif and in C-terminal regulatory extension.
MPK9 and MPK12 (show MAPK12 Antibodies) function redundantly downstream of extracellular reactive oxygen production and intracellular accumulation, cytosolic alkalisation and Ca(2 (show CA2 Antibodies)+)cytosolic oscillation in yeast elcictor-induced stomatal closure
MPK9 and MPK12 (show MAPK12 Antibodies) act downstream of ROS (show ROS1 Antibodies) and cytosolic Ca2 (show CA2 Antibodies)+ and upstream of anion channels in the guard cell abscisic acid signaling cascade.
MAP kinases MPK9 and MPK12 (show MAPK12 Antibodies) are preferentially expressed in guard cells and positively regulate ROS (show ROS1 Antibodies)-mediated ABA signaling.
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 targets specific transcription factors, and thus mediates immediate-early gene expression in response to various cell stimuli. It is most closely related to MAPK8, both of which are involved in UV radiation induced apoptosis, thought to be related to the cytochrome c-mediated cell death pathway. This gene and MAPK8 are also known as c-Jun N-terminal kinases. This kinase blocks the ubiquitination of tumor suppressor p53, and thus it increases the stability of p53 in nonstressed cells. Studies of this gene's mouse counterpart suggest a key role in T-cell differentiation. Several alternatively spliced transcript variants encoding distinct isoforms have been reported.
mitogen-activated protein kinase 9
, Jun kinase
, MAP kinase 9
, MAPK 9
, c-Jun N-terminal kinase 2
, c-Jun kinase 2
, stress-activated protein kinase 1a
, stress-activated protein kinase JNK2
, JNK/SAPK alpha
, mitogen activated protein kinase 9
, protein kinase, mitogen-activated 9
, stress activated protein kinase alpha II
, janus kinase 2
, c-JUN amino-terminal kinase-2 alpha1