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Human Polyclonal MAPK14 Primary Antibody für 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 für 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 für 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 (zeige MAPK1 Antikörper) 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 (zeige MYC Antikörper) and NOTCH (zeige NOTCH1 Antikörper) signaling, demonstrate two mechanisms of NOTCH3 (zeige NOTCH3 Antikörper) regulation and provide evidence for NOTCH3 (zeige NOTCH3 Antikörper) involvement in prostate luminal cell differentiation.
Overall, these results suggest that p53 (zeige TP53 Antikörper) is involved in improving insulin (zeige INS Antikörper) sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB (zeige NFKB1 Antikörper) pathways.
Data show that the combination of targeting RAD51 (zeige RAD51 Antikörper) and p38 (zeige CRK Antikörper) inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1 (zeige PARP1 Antikörper).
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 (zeige CRK Antikörper)-p38IP (zeige SUPT20H Antikörper) is required for the Snail (zeige SNAI1 Antikörper)-induced E-cadherin (zeige CDH1 Antikörper) down-regulation and cell invasion in HNSCC
GATA4 (zeige GATA4 Antikörper) is a regulator of osteoblastic differentiation via the p38 (zeige CRK Antikörper) signaling pathways.
CX3CL1 (zeige CX3CL1 Antikörper)/CX3CR1 (zeige CX3CR1 Antikörper) 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 (zeige CD8A Antikörper)+ Tregs depended in part on transforming growth factor beta 1 (TGF-beta1 (zeige TGFB1 Antikörper)) 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 (zeige GADD45B Antikörper) rs2024144T, MAPK14 rs3804451A and GADD45A (zeige GADD45A Antikörper) rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
results suggest that ET-1 (zeige EDN1 Antikörper)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (zeige NOX1 Antikörper)-PKCalpha (zeige PKCa Antikörper)-p(38)MAPK (zeige MAPK1 Antikörper) and NFkappaB-MT1MMP (zeige MMP14 Antikörper) signaling pathways along with a marked decrease in TIMP-2 (zeige TIMP2 Antikörper) expression in the cells
cross-talk between p(38)MAPK (zeige MAPK1 Antikörper) and Gialpha play a pivotal role for full activation of cPLA2 (zeige PLA2G4A Antikörper) during ET-1 (zeige EDN1 Antikörper) 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 (zeige MMP13 Antikörper) 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 (zeige MAPK8 Antikörper) 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 (zeige SLC12A1 Antikörper) involves activation of p38 and JNK (zeige MAPK8 Antikörper) MAPKs
These data suggest a differential requirement of JNK1 (zeige MAPK8 Antikörper) and p38 MAPK in TNF (zeige TNF Antikörper) regulation of E2F1 (zeige E2F1 Antikörper). Targeted inactivation of JNK1 (zeige MAPK8 Antikörper) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (zeige TNF Antikörper)-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 (zeige JAK3 Antikörper) signalling in a Drosophila model of Myeloproliferative neoplasms.
ROS (zeige ROS1 Antikörper)/JNK (zeige MAPK8 Antikörper)/p38/Upd (zeige UROD Antikörper) 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 (zeige MAPK1 Antikörper) and Rack1 (zeige GNB2L1 Antikörper) 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 (zeige MAPK1 Antikörper) 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 (zeige MAPK1 Antikörper) 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 (zeige ZBED1 Antikörper) pathway and DREF (zeige ZBED1 Antikörper) is involved in the regulation of proliferation and differentiation of Drosophila ISCs (zeige NFS1 Antikörper) and progenitors
The Macrophage Activation Induced by Bacillus thuringiensis Cry1Ac Protoxin Involves ERK1/2 and p38 (zeige CRK Antikörper) Pathways and the Interaction with Cell-Surface-HSP70 (zeige HSP70 Antikörper)
MAPK (zeige MAPK1 Antikörper) in, and found that p38alpha deficiency causes Th1 (zeige HAND1 Antikörper) cells to hyperproliferate via the Mnk1 (zeige MKNK1 Antikörper)/eIF4E (zeige EIF4E Antikörper) pathway
B7-H1 (zeige CD274 Antikörper) suppresses p38 MAPK activation by sequestering DNA-PKcs (zeige PRKDC Antikörper) in order to preserve T cell survival
increased in lentivirus vector thioredoxin interacting protein (zeige TXNIP Antikörper) (LV-GFP-TXNIP (zeige TXNIP Antikörper)) cells.
Our data demonstrated that p38 MAPK may be a potential therapeutic target for hypertension-related cognitive dysfunction.
MKK4 (zeige MAP2K4 Antikörper) is the major MAP2K, which activates JNK (zeige MAPK8 Antikörper) in acute liver injury. p38 (zeige CRK Antikörper), the other downstream target of MKK4 (zeige MAP2K4 Antikörper), does not contribute to liver injury from APAP or TNF (zeige TNF Antikörper)/galactosamine.
Endogenous hydrogen sulfide (zeige SQRDL Antikörper)-mediated MAPK (zeige MAPK1 Antikörper) inhibition preserves endothelial function through TXNIP (zeige TXNIP Antikörper) signaling.
Suppressing P38 (zeige CRK Antikörper) 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 (zeige MAPK8 Antikörper) 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 (zeige PKCd Antikörper)-TIRAP (zeige TIRAP Antikörper)-p38 (zeige CRK Antikörper)) in proinflammatory cytokine expression, which controls the development of the inflammatory trigger in stimulated macrophages.
CXCL13 (zeige CXCL13 Antikörper) acts on CXCR5 (zeige CXCR5 Antikörper) to increase p38 (zeige CRK Antikörper) activation and further contributes to the pathogenesis of orofacial neuropathic pain
cytochrome c (zeige CYCS Antikörper) microinjection induces p38 phosphorylation through caspase-3 (zeige CASP3 Antikörper) activation, and caspase (zeige CASP3 Antikörper) 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 (zeige MAPK1 Antikörper)) is essential for drug-induced COX-2 (zeige PTGS2 Antikörper) 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 (zeige IL10 Antikörper) production through p38 MAPK activation.
JNK (zeige MAPK8 Antikörper) 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 (zeige ROS1 Antikörper) causes dedifferentiation through the ERK (zeige MAPK1 Antikörper) 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 (zeige NFKB1 Antikörper), p53 (zeige TP53 Antikörper) and caspase-3 (zeige CASP3 Antikörper) activation.
P38 and JNK (zeige MAPK8 Antikörper) have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
Adult zebrafish cardiomyocytes express active p38alpha MAPK (zeige MAPK1 Antikörper), which is switched off upon entry into mitosis.
Dkk3r regulates p38a phosphorylation to maintain Smad4 (zeige SMAD4 Antikörper) stability, in turn enabling the Smad2 (zeige SMAD2 Antikörper).Smad3a.Smad4 complex to form and activate the myf5 (zeige MYF5 Antikörper) 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