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Human Polyclonal MAPK14 Primary Antibody for FACS, IF - ABIN1882176
Cheung, Campbell, Nebreda, Cohen: Feedback control of the protein kinase TAK1 by SAPK2a/p38alpha. in The EMBO journal 2003
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Human Monoclonal MAPK14 Primary Antibody for IHC, ELISA - ABIN1724904
Li, Zheng, Li, Ma: Unfractionated heparin inhibits lipopolysaccharide-induced inflammatory response through blocking p38 MAPK and NF-?B activation on endothelial cell. in Cytokine 2012
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Human Monoclonal MAPK14 Primary Antibody for ICC, FACS - ABIN1724830
Chung, Tang, Sun, Chou, Yeh, Yu, Sun: Galectin-1 promotes lung cancer progression and chemoresistance by upregulating p38 MAPK, ERK, and cyclooxygenase-2. in Clinical cancer research : an official journal of the American Association for Cancer Research 2012
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hepatic p38alpha MAPK (show MAPK1 Antibodies) functions as a negative regulator of liver steatosis in maintaining hepatic bile acid synthesis and fatty acid beta-oxidation by antagonizing the c-Jun N-terminal kinase (JNK).
The results reveal a new connection between p38MAPK, MYC (show MYC Antibodies) and NOTCH (show NOTCH1 Antibodies) signaling, demonstrate two mechanisms of NOTCH3 (show NOTCH3 Antibodies) regulation and provide evidence for NOTCH3 (show NOTCH3 Antibodies) involvement in prostate luminal cell differentiation.
Overall, these results suggest that p53 (show TP53 Antibodies) is involved in improving insulin (show INS Antibodies) sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB (show NFKB1 Antibodies) pathways.
Data show that the combination of targeting RAD51 (show RAD51 Antibodies) and p38 (show CRK Antibodies) inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1 (show PARP1 Antibodies).
Fas-FasL is the preferred death pathway for both Th1 and Th17 and that inherently low Erk2 activity protected Th17 cells from TCR AICD.
provide the first report that p38 (show CRK Antibodies)-p38IP (show SUPT20H Antibodies) is required for the Snail (show SNAI1 Antibodies)-induced E-cadherin (show CDH1 Antibodies) down-regulation and cell invasion in HNSCC
GATA4 (show GATA4 Antibodies) is a regulator of osteoblastic differentiation via the p38 (show CRK Antibodies) signaling pathways.
CX3CL1 (show CX3CL1 Antibodies)/CX3CR1 (show CX3CR1 Antibodies) axis plays a key role in the development of ischemia-induced oligodendrocyte injury via p38MAPK signaling pathway.
Data suggest that in vitro-induction of CD8 (show CD8A Antibodies)+ Tregs depended in part on transforming growth factor beta 1 (TGF-beta1 (show TGFB1 Antibodies)) activation of p38 MAPK signaling, and that p38 MAPK could be a therapeutic target in ovarian cancer (OC) anti-tumor immunotherapy.
present study provides evidence that variations in GADD45B (show GADD45B Antibodies) rs2024144T, MAPK14 rs3804451A and GADD45A (show GADD45A Antibodies) rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
results suggest that ET-1 (show EDN1 Antibodies)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (show NOX1 Antibodies)-PKCalpha (show PKCa Antibodies)-p(38)MAPK (show MAPK1 Antibodies) and NFkappaB-MT1MMP (show MMP14 Antibodies) signaling pathways along with a marked decrease in TIMP-2 (show TIMP2 Antibodies) expression in the cells
cross-talk between p(38)MAPK (show MAPK1 Antibodies) and Gialpha play a pivotal role for full activation of cPLA2 (show PLA2G4A Antibodies) during ET-1 (show EDN1 Antibodies) stimulation of pulmonary artery smooth muscle cells.
MAPK14 signalling pathway is largely involved in heat-induced sperm damage.
p38 MAPK is an early redox sensor in the laminar shear stress with hydrogen peroxide being a signaling mediator.
Blockade of p38 enhances chondrocyte phenotype in monolayer culture and may promote more efficient cartilage tissue regeneration for cell-based therapies.
p38 phosphorylation and MMP13 (show MMP13 Antibodies) expression are regulated by Rho/ROCK activation, and support the potential novel pathway that Rho/ROCK is in the upper part of the mechanical stress-induced matrix degeneration cascade in cartilage.
These data suggest that the p38 and JNK (show MAPK8 Antibodies) signaling pathways play pivotal roles in PRRSV replication and may regulate immune responses during virus infection.
findings support the hypothesis that ischemic factor stimulation of the blood-brain barrier Na-K-Cl cotransporter (show SLC12A1 Antibodies) involves activation of p38 and JNK (show MAPK8 Antibodies) MAPKs
These data suggest a differential requirement of JNK1 (show MAPK8 Antibodies) and p38 MAPK in TNF (show TNF Antibodies) regulation of E2F1 (show E2F1 Antibodies). Targeted inactivation of JNK1 (show MAPK8 Antibodies) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (show TNF Antibodies)-mediated EC dysfunction.
p38 MAPK (MAPK14) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.
These results illustrate a novel pro-tumourigenic crosstalk between the p38 MAPK pathway and JAK (show JAK3 Antibodies) signalling in a Drosophila model of Myeloproliferative neoplasms.
ROS (show ROS1 Antibodies)/JNK (show MAPK8 Antibodies)/p38/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.
Taken together, our findings indicate that the p38 MAP Kinase is an integral component of the core circadian clock of Drosophila in addition to playing a role in stress-input pathways.
Data show that the genetic interaction between p38b MAPK (show MAPK1 Antibodies) and Rack1 (show GNB2L1 Antibodies) controls muscle aggregate formation, locomotor function, and longevity.
The interaction of any of several Drosophila Delta class glutathione transferases and p38b mitogen-activated protein kinase (show MAPK1 Antibodies) can affect the substrate specificity of either enzyme, which suggests induced conformational changes affecting catalysis.
found a correlation between the depth of integration of individual p38 kinases into the protein interaction network and their functional significance; propose a central role of p38b in the p38 signaling module with p38a and p38c playing more peripheral auxiliary roles
Loss of p38 MAPK causes early lethality and precipitates age-related motor dysfunction and stress sensitivity.
The p38 pathway-mediated stress response contribute to Drosophila host defense against microbial infection.
p38b MAPK (show MAPK1 Antibodies) plays a crucial role in the balance between intestinal stem cell proliferation and proper differentiation in the adult Drosophila midgut.
the D-p38b gene is regulated by the DREF (show ZBED1 Antibodies) pathway and DREF (show ZBED1 Antibodies) is involved in the regulation of proliferation and differentiation of Drosophila ISCs (show NFS1 Antibodies) and progenitors
The Macrophage Activation Induced by Bacillus thuringiensis Cry1Ac Protoxin Involves ERK1/2 and p38 (show CRK Antibodies) Pathways and the Interaction with Cell-Surface-HSP70 (show HSP70 Antibodies)
MAPK (show MAPK1 Antibodies) in, and found that p38alpha deficiency causes Th1 (show HAND1 Antibodies) cells to hyperproliferate via the Mnk1 (show MKNK1 Antibodies)/eIF4E (show EIF4E Antibodies) pathway
B7-H1 (show CD274 Antibodies) suppresses p38 MAPK activation by sequestering DNA-PKcs (show PRKDC Antibodies) in order to preserve T cell survival
increased in lentivirus vector thioredoxin interacting protein (show TXNIP Antibodies) (LV-GFP-TXNIP (show TXNIP Antibodies)) cells.
Our data demonstrated that p38 MAPK may be a potential therapeutic target for hypertension-related cognitive dysfunction.
MKK4 (show MAP2K4 Antibodies) is the major MAP2K, which activates JNK (show MAPK8 Antibodies) in acute liver injury. p38 (show CRK Antibodies), the other downstream target of MKK4 (show MAP2K4 Antibodies), does not contribute to liver injury from APAP or TNF (show TNF Antibodies)/galactosamine.
Endogenous hydrogen sulfide (show SQRDL Antibodies)-mediated MAPK (show MAPK1 Antibodies) inhibition preserves endothelial function through TXNIP (show TXNIP Antibodies) signaling.
Suppressing P38 (show CRK Antibodies) 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 (show MAPK8 Antibodies) weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis.
Our key findings provide novel insights into the mechanism of action of heterotrimeric complex (PKCdelta (show PKCd Antibodies)-TIRAP (show TIRAP Antibodies)-p38 (show CRK Antibodies)) in proinflammatory cytokine expression, which controls the development of the inflammatory trigger in stimulated macrophages.
CXCL13 (show CXCL13 Antibodies) acts on CXCR5 (show CXCR5 Antibodies) to increase p38 (show CRK Antibodies) activation and further contributes to the pathogenesis of orofacial neuropathic pain
cytochrome c (show CYCS Antibodies) microinjection induces p38 phosphorylation through caspase-3 (show CASP3 Antibodies) activation, and caspase (show CASP3 Antibodies) inhibition reduces p38 activation induced by osmostress, indicating that a positive feedback loop is engaged by hyperosmotic shock
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (show MAPK1 Antibodies)) is essential for drug-induced COX-2 (show PTGS2 Antibodies) expression in leukocytes, suggesting that p38 MAPK is a potential target for anti-inflammatory therapy.
These findings support a function for p38 MAPK in equine neutrophil migration and suggest the potential for the ability of p38 MAPK inhibition to limit neutrophilic inflammation in the laminae during acute laminitis.
Cultured equine digital vein endothelial cells were exposed to lipopolysaccharide and phosphorylation of p38 MAPK was assessed by Western blotting using phospho-specific antibodies.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (show IL10 Antibodies) production through p38 MAPK activation.
JNK (show MAPK8 Antibodies) plays an active role in fragmentation of pig oocytes and p38 MAPK is not involved in this process.[p38MAPK]
Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries.
These findings suggest that the TQ-induced production of ROS (show ROS1 Antibodies) causes dedifferentiation through the ERK (show MAPK1 Antibodies) pathway and inflammation through the PI3K and p38 pathways in rabbit articular chondrocytes.
These results suggest that p38 MAPK signal transduction pathway is critical to NO-induced chondrocyte apoptosis, and p38 plays a role by way of stimulating NF-kappaB (show NFKB1 Antibodies), p53 (show TP53 Antibodies) and caspase-3 (show CASP3 Antibodies) activation.
P38 and JNK (show MAPK8 Antibodies) have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
Adult zebrafish cardiomyocytes express active p38alpha MAPK (show MAPK1 Antibodies), which is switched off upon entry into mitosis.
Dkk3r regulates p38a phosphorylation to maintain Smad4 (show SMAD4 Antibodies) stability, in turn enabling the Smad2 (show SMAD2 Antibodies).Smad3a.Smad4 complex to form and activate the myf5 (show MYF5 Antibodies) promoter.
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 environmental stresses and proinflammatory cytokines. The activation requires its phosphorylation by MAP kinase kinases (MKKs), or its autophosphorylation triggered by the interaction of MAP3K7IP1/TAB1 protein with this kinase. The substrates of this kinase include transcription regulator ATF2, MEF2C, and MAX, cell cycle regulator CDC25B, and tumor suppressor p53, which suggest the roles of this kinase in stress related transcription and cell cycle regulation, as well as in genotoxic stress response. Four alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.
Csaids binding protein
, MAP kinase 14
, MAP kinase 2
, MAP kinase Mxi2
, MAP kinase p38 alpha
, MAPK 14
, MAX-interacting protein 2
, cytokine suppressive anti-inflammatory drug binding protein
, cytokine-supressive anti-inflammatory drug binding protein
, mitogen-activated protein kinase 14
, mitogen-activated protein kinase 14A
, mitogen-activated protein kinase p38 alpha
, p38 MAP kinase
, p38 mitogen activated protein kinase
, p38alpha Exip
, reactive kinase
, stress-activated protein kinase 2A
, p38 mitogen-activated protein kinase
, stress-activated p38b MAP kinase
, cytokine suppressive anti-inflammatory drug binding protein 1
, mitogen activated protein kinase 14
, p38 MAP kinase alpha
, p38 MAPK
, p38 alpha
, tRNA synthetase cofactor p38
, MAPK p38
, Mitogen-activated protein kinase 2
, mitogen-activated Mitogen-activated protein kinase 2
, p38 mitogen-activated kinase
, CSAIDS-binding protein 1
, stress-activated protein kinase 2a
, MAP kinase 14A
, MAP kinase p38a
, MAPK 14A
, Mitogen-activated protein kinase p38a
, mitogen-activated protein kinase p38a