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抗Human MAPK14 抗体:
抗Mouse (Murine) MAPK14 抗体:
抗Rat (Rattus) MAPK14 抗体:
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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Dog (Canine) Monoclonal MAPK14 Primary Antibody for IF, WB - ABIN968769
Brunet, Pouysségur: Identification of MAP kinase domains by redirecting stress signals into growth factor responses. in Science (New York, N.Y.) 1996
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Dog (Canine) Monoclonal MAPK14 Primary Antibody for IF, WB - ABIN968770
Han, Lee, Bibbs, Ulevitch: A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. in Science (New York, N.Y.) 1994
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Human Monoclonal MAPK14 Primary Antibody for ICC, FACS - ABIN1724830
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 IHC, ELISA - ABIN1724904
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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results suggest that ET-1 (显示 EDN1 抗体)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (显示 NOX1 抗体)-PKCalpha (显示 PKCa 抗体)-p(38)MAPK (显示 MAPK1 抗体) and NFkappaB-MT1MMP (显示 MMP14 抗体) signaling pathways along with a marked decrease in TIMP-2 (显示 TIMP2 抗体) expression in the cells
cross-talk between p(38)MAPK (显示 MAPK1 抗体) and Gialpha play a pivotal role for full activation of cPLA2 (显示 PLA2G4A 抗体) during ET-1 (显示 EDN1 抗体) 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 (显示 MMP13 抗体) 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 (显示 MAPK8 抗体) 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 (显示 SLC12A1 抗体) involves activation of p38 and JNK (显示 MAPK8 抗体) MAPKs
These data suggest a differential requirement of JNK1 (显示 MAPK8 抗体) and p38 MAPK in TNF (显示 TNF 抗体) regulation of E2F1 (显示 E2F1 抗体). Targeted inactivation of JNK1 (显示 MAPK8 抗体) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (显示 TNF 抗体)-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 (显示 JAK3 抗体) signalling in a Drosophila model of Myeloproliferative neoplasms.
ROS (显示 ROS1 抗体)/JNK (显示 MAPK8 抗体)/p38/Upd (显示 UROD 抗体) 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 (显示 MAPK1 抗体) and Rack1 (显示 GNB2L1 抗体) 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 (显示 MAPK1 抗体) 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 (显示 MAPK1 抗体) 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 (显示 ZBED1 抗体) pathway and DREF (显示 ZBED1 抗体) is involved in the regulation of proliferation and differentiation of Drosophila ISCs (显示 NFS1 抗体) and progenitors
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (显示 MAPK1 抗体)) is essential for drug-induced COX-2 (显示 PTGS2 抗体) 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.
Data show that the combination of targeting RAD51 (显示 RAD51 抗体) and p38 (显示 CRK 抗体) inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1 (显示 PARP1 抗体).
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 (显示 CRK 抗体)-p38IP (显示 SUPT20H 抗体) is required for the Snail (显示 SNAI1 抗体)-induced E-cadherin (显示 CDH1 抗体) down-regulation and cell invasion in HNSCC
GATA4 (显示 GATA4 抗体) is a regulator of osteoblastic differentiation via the p38 (显示 CRK 抗体) signaling pathways.
CX3CL1 (显示 CX3CL1 抗体)/CX3CR1 (显示 CX3CR1 抗体) 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 (显示 CD8A 抗体)+ Tregs depended in part on transforming growth factor beta 1 (TGF-beta1 (显示 TGFB1 抗体)) 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 (显示 GADD45B 抗体) rs2024144T, MAPK14 rs3804451A and GADD45A (显示 GADD45A 抗体) rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
Gab1 (显示 GAB1 抗体)/SHP2 (显示 PTPN11 抗体)/p38MAPK signaling pathway and Ang-2 (显示 ANGPT2 抗体) have an essential role in regulating thrombin (显示 F2 抗体)-induced monocyte adhesion and vascular leakage
Studies suugest Wip1 (显示 PPM1D 抗体) role in tumorigenesis through regulation of p53 (显示 TP53 抗体) and p38MAPK pathways.
Data show that Cx43 (显示 GJA1 抗体) was inhibited predominantly via IL-1beta (显示 IL1B 抗体)-activated ERK1/2 (显示 MAPK1/3 抗体) and p38 MAP kinase cascades.
Macrophage p38alpha-deficient mice had decreased mortality and GalN (显示 GAL 抗体)/TNF-alpha (显示 TNF 抗体)-induced liver injury apoptosis, less apoptosis, accelerated regeneration, decreased granulocyte recruitment, monocytes infiltration, and cytokine production after GalN (显示 GAL 抗体)/TNF-alpha (显示 TNF 抗体) treatment. Mechanistically, p38 (显示 CRK 抗体) signaling was activated by lipopolysaccharide/interferon-gamma (显示 IFNG 抗体) treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibi
results suggest that the TLR2 (显示 TLR2 抗体)-p38 (显示 CRK 抗体)-CD86 (显示 CD86 抗体) signaling pathway plays a vital role in inflammation associated with burn injury
Overall, our results provide the first evidence that HDAC6 (显示 HDAC6 抗体) is capable of inducing expression of pro-inflammatory genes by regulating the ROS (显示 ROS1 抗体)-MAPK (显示 MAPK1 抗体)-NF-kappaB (显示 NFKB1 抗体)/AP-1 (显示 JUN 抗体) pathways and serves as a molecular target for inflammation.
YZH-106 induced p38 MAPK and ERK1/2 (显示 MAPK1/3 抗体) phosphorylation, which led to the activation of erythroid 2-related factor 2 (Nrf2 (显示 NFE2L2 抗体)) that up-regulated heme oxygenase-1 (HO-1 (显示 HMOX1 抗体)) expression in addition to other genes.
Trehalose may rescue against insulin (显示 INS 抗体) resistance-induced myocardial contractile defect and apoptosis, via autophagy associated with dephosphorylation of p38 MAPK and Foxo1 (显示 FOXO1 抗体) without affecting phosphorylation of Akt (显示 AKT1 抗体).
SPAK (显示 STK39 抗体) plays a pathogenic role in IgA nephropathy through the activation of NF-kappaB (显示 NFKB1 抗体)/MAPK (显示 MAPK1 抗体) signaling pathway.
cyclophilin (显示 PPIE 抗体)-dependent isomerisation of p38MAPK is an important novel mechanism in regulating p38MAPK phosphorylation and functions.
findings identify p38alpha MAPK (显示 MAPK1 抗体) as a key component of PTH (显示 PTH 抗体) signaling in osteoblast lineage cells and highlight its requirement in iPTH osteoanabolic activity
p38alpha serves as a critical regulator of platelet activation and potential indicator of highly thrombotic lesions and no-reflow in ST-elevation myocardial infarction.
Blockade of TRPV1 (显示 TRPV1 抗体), through genetic deletion or systemic or intra-nucleus accumbens (NAc (显示 NLRP1 抗体)) pharmacological means, inhibited morphine-induced CPP in mice. In addition, p38 MAPK inhibition blocked development of morphine conditioned place preference (CPP) as well. Moreover, blockade of either NAc (显示 NLRP1 抗体) p38 MAPK or TRPV1 (显示 TRPV1 抗体) dampened protein expression levels of p-p38 MAPK, AC1 (显示 HRASLS 抗体), and p-NF-kappaB (显示 NFKB1 抗体) which are normally induced by morphine ...
These findings suggest that the TQ-induced production of ROS (显示 ROS1 抗体) causes dedifferentiation through the ERK (显示 MAPK1 抗体) 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 (显示 NFKB1 抗体), p53 (显示 TP53 抗体) and caspase-3 (显示 CASP3 抗体) activation.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (显示 IL10 抗体) production through p38 MAPK activation.
JNK (显示 MAPK8 抗体) 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 (显示 MAPK1/3 抗体), in the neuroretina and retinal arteries.
cytochrome c (显示 CYCS 抗体) microinjection induces p38 phosphorylation through caspase-3 (显示 CASP3 抗体) activation, and caspase (显示 CASP3 抗体) 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