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anti-Human MAPK14 Anticorps:
anti-Mouse (Murine) MAPK14 Anticorps:
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Human Polyclonal MAPK14 Primary Antibody pour FACS, IF - ABIN1882176
Cheung, Campbell, Nebreda, Cohen: Feedback control of the protein kinase TAK1 by SAPK2a/p38alpha. dans The EMBO journal 2003
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Dog (Canine) Monoclonal MAPK14 Primary Antibody pour IF, WB - ABIN968769
Brunet, Pouysségur: Identification of MAP kinase domains by redirecting stress signals into growth factor responses. dans Science (New York, N.Y.) 1996
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Dog (Canine) Monoclonal MAPK14 Primary Antibody pour IF, WB - ABIN968770
Han, Lee, Bibbs, Ulevitch: A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. dans Science (New York, N.Y.) 1994
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Human Monoclonal MAPK14 Primary Antibody pour 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. dans Cytokine 2012
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Human Monoclonal MAPK14 Primary Antibody pour 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. dans Clinical cancer research : an official journal of the American Association for Cancer Research 2012
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results suggest that ET-1 (Montrer EDN1 Anticorps)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (Montrer NOX1 Anticorps)-PKCalpha (Montrer PKCa Anticorps)-p(38)MAPK (Montrer MAPK1 Anticorps) and NFkappaB-MT1MMP (Montrer MMP14 Anticorps) signaling pathways along with a marked decrease in TIMP-2 (Montrer TIMP2 Anticorps) expression in the cells
cross-talk between p(38)MAPK (Montrer MAPK1 Anticorps) and Gialpha play a pivotal role for full activation of cPLA2 (Montrer PLA2G4A Anticorps) during ET-1 (Montrer EDN1 Anticorps) 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 (Montrer MMP13 Anticorps) 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 (Montrer MAPK8 Anticorps) 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 (Montrer SLC12A1 Anticorps) involves activation of p38 and JNK (Montrer MAPK8 Anticorps) MAPKs
These data suggest a differential requirement of JNK1 (Montrer MAPK8 Anticorps) and p38 MAPK in TNF (Montrer TNF Anticorps) regulation of E2F1 (Montrer E2F1 Anticorps). Targeted inactivation of JNK1 (Montrer MAPK8 Anticorps) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (Montrer TNF Anticorps)-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 (Montrer JAK3 Anticorps) signalling in a Drosophila model of Myeloproliferative neoplasms.
ROS (Montrer ROS1 Anticorps)/JNK (Montrer MAPK8 Anticorps)/p38/Upd (Montrer UROD Anticorps) 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 (Montrer MAPK1 Anticorps) and Rack1 (Montrer GNB2L1 Anticorps) 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 (Montrer MAPK1 Anticorps) 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 (Montrer MAPK1 Anticorps) 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 (Montrer ZBED1 Anticorps) pathway and DREF (Montrer ZBED1 Anticorps) is involved in the regulation of proliferation and differentiation of Drosophila ISCs (Montrer NFS1 Anticorps) and progenitors
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (Montrer MAPK1 Anticorps)) is essential for drug-induced COX-2 (Montrer PTGS2 Anticorps) 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.
Overall, these results suggest that p53 (Montrer TP53 Anticorps) is involved in improving insulin (Montrer INS Anticorps) sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB (Montrer NFKB1 Anticorps) pathways.
Data show that the combination of targeting RAD51 (Montrer RAD51 Anticorps) and p38 (Montrer CRK Anticorps) inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1 (Montrer PARP1 Anticorps).
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 (Montrer CRK Anticorps)-p38IP (Montrer SUPT20H Anticorps) is required for the Snail (Montrer SNAI1 Anticorps)-induced E-cadherin (Montrer CDH1 Anticorps) down-regulation and cell invasion in HNSCC
GATA4 (Montrer GATA4 Anticorps) is a regulator of osteoblastic differentiation via the p38 (Montrer CRK Anticorps) signaling pathways.
CX3CL1 (Montrer CX3CL1 Anticorps)/CX3CR1 (Montrer CX3CR1 Anticorps) 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 (Montrer CD8A Anticorps)+ Tregs depended in part on transforming growth factor beta 1 (TGF-beta1 (Montrer TGFB1 Anticorps)) 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 (Montrer GADD45B Anticorps) rs2024144T, MAPK14 rs3804451A and GADD45A (Montrer GADD45A Anticorps) rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
Gab1/SHP2 (Montrer PTPN11 Anticorps)/p38MAPK signaling pathway and Ang-2 (Montrer ANGPT2 Anticorps) have an essential role in regulating thrombin (Montrer F2 Anticorps)-induced monocyte adhesion and vascular leakage
Studies suugest Wip1 (Montrer PPM1D Anticorps) role in tumorigenesis through regulation of p53 (Montrer TP53 Anticorps) and p38MAPK pathways.
p38 (Montrer CRK Anticorps) role in the Helicobacter pylori podocyte infiltration
Our data suggest that rCC16 suppresses LPS (Montrer TLR4 Anticorps)-mediated inflammatory mediator TNF-alpha (Montrer TNF Anticorps), IL-6 (Montrer IL6 Anticorps), and IL-8 (Montrer IL8 Anticorps) production by inactivating NF-kappaB (Montrer NFKB1 Anticorps) and p38 MAPK but not AP-1 (Montrer JUN Anticorps) in RAW264.7 cells.
high fat diet (HFD) and zinc deficiency synergistically induce obesity-related cardiac hypertrophy (ORCH), by increasing oxidative stress-mediated activation of BCL10 (Montrer BCL10 Anticorps)/CARD9 (Montrer CARD9 Anticorps)/p38 MAPK signalling. Zinc supplement ameliorates ORCH through activation of metallothionein (Montrer MT Anticorps) to repress oxidative stress-activated BCL10 (Montrer BCL10 Anticorps) expression and p38 MAPK activation.
involvement of CacyBP/SIP (Montrer CACYBP Anticorps) in the regulation of p38 (Montrer CRK Anticorps) kinase activity, in addition to that of ERK1/2, might point to the function of CacyBP/SIP (Montrer CACYBP Anticorps) in pro-survival and pro-apoptotic pathways.
Macrophage p38alpha-deficient mice had decreased mortality and GalN (Montrer GAL Anticorps)/TNF-alpha (Montrer TNF Anticorps)-induced liver injury apoptosis, less apoptosis, accelerated regeneration, decreased granulocyte recruitment, monocytes infiltration, and cytokine production after GalN (Montrer GAL Anticorps)/TNF-alpha (Montrer TNF Anticorps) treatment. Mechanistically, p38 (Montrer CRK Anticorps) signaling was activated by lipopolysaccharide/interferon-gamma (Montrer IFNG Anticorps) treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibi
results suggest that the TLR2-p38 (Montrer CRK Anticorps)-CD86 (Montrer CD86 Anticorps) signaling pathway plays a vital role in inflammation associated with burn injury
Overall, our results provide the first evidence that HDAC6 (Montrer HDAC6 Anticorps) is capable of inducing expression of pro-inflammatory genes by regulating the ROS (Montrer ROS1 Anticorps)-MAPK (Montrer MAPK1 Anticorps)-NF-kappaB (Montrer NFKB1 Anticorps)/AP-1 (Montrer JUN Anticorps) pathways and serves as a molecular target for inflammation.
YZH-106 induced p38 MAPK and ERK1/2 phosphorylation, which led to the activation of erythroid 2-related factor 2 (Nrf2 (Montrer NFE2L2 Anticorps)) that up-regulated heme oxygenase-1 (HO-1 (Montrer HMOX1 Anticorps)) expression in addition to other genes.
Trehalose may rescue against insulin (Montrer INS Anticorps) resistance-induced myocardial contractile defect and apoptosis, via autophagy associated with dephosphorylation of p38 MAPK and Foxo1 (Montrer FOXO1 Anticorps) without affecting phosphorylation of Akt (Montrer AKT1 Anticorps).
These findings suggest that the TQ-induced production of ROS (Montrer ROS1 Anticorps) causes dedifferentiation through the ERK (Montrer MAPK1 Anticorps) 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 (Montrer NFKB1 Anticorps), p53 (Montrer TP53 Anticorps) and caspase-3 (Montrer CASP3 Anticorps) activation.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (Montrer IL10 Anticorps) production through p38 MAPK activation.
JNK (Montrer MAPK8 Anticorps) 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.
cytochrome c (Montrer CYCS Anticorps) microinjection induces p38 phosphorylation through caspase-3 (Montrer CASP3 Anticorps) activation, and caspase (Montrer CASP3 Anticorps) inhibition reduces p38 activation induced by osmostress, indicating that a positive feedback loop is engaged by hyperosmotic shock
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.
MAP kinase 14
, MAP kinase p38 alpha
, MAPK 14
, mitogen-activated protein kinase p38 alpha
, p38 mitogen activated protein kinase
, p38 mitogen-activated protein kinase
, stress-activated p38b MAP kinase
, p38 mitogen-activated 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
, CSAIDS-binding protein 1
, mitogen-activated protein kinase 14A
, stress-activated protein kinase 2a
, Csaids binding protein
, MAP kinase 2
, MAP kinase Mxi2
, MAX-interacting protein 2
, cytokine suppressive anti-inflammatory drug binding protein
, cytokine-supressive anti-inflammatory drug binding protein
, mitogen-activated protein kinase 14
, p38 MAP kinase
, p38alpha Exip
, reactive kinase
, stress-activated protein kinase 2A
, MAPK p38
, Mitogen-activated protein kinase 2
, mitogen-activated Mitogen-activated protein kinase 2