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Human MAPK14 Protein expressed in Baculovirus infected Insect Cells - ABIN2002027
Tamura, Sudo, Senftleben, Dadak, Johnson, Karin: Requirement for p38alpha in erythropoietin expression: a role for stress kinases in erythropoiesis. in Cell 2000
Show all 4 Pubmed References
results suggest that ET-1 (show EDN1 Proteins)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (show NOX1 Proteins)-PKCalpha (show PKCa Proteins)-p(38)MAPK (show MAPK1 Proteins) and NFkappaB-MT1MMP (show MMP14 Proteins) signaling pathways along with a marked decrease in TIMP-2 (show TIMP2 Proteins) expression in the cells
cross-talk between p(38)MAPK (show MAPK1 Proteins) and Gialpha play a pivotal role for full activation of cPLA2 (show PLA2G4A Proteins) during ET-1 (show EDN1 Proteins) 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 Proteins) 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 Proteins) 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 Proteins) involves activation of p38 and JNK (show MAPK8 Proteins) MAPKs
These data suggest a differential requirement of JNK1 (show MAPK8 Proteins) and p38 MAPK in TNF (show TNF Proteins) regulation of E2F1 (show E2F1 Proteins). Targeted inactivation of JNK1 (show MAPK8 Proteins) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (show TNF Proteins)-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 Proteins) signalling in a Drosophila model of Myeloproliferative neoplasms.
ROS (show ROS1 Proteins)/JNK (show MAPK8 Proteins)/p38/Upd (show UROD Proteins) 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 Proteins) and Rack1 (show GNB2L1 Proteins) 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 Proteins) 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 Proteins) 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 Proteins) pathway and DREF (show ZBED1 Proteins) is involved in the regulation of proliferation and differentiation of Drosophila ISCs (show NFS1 Proteins) and progenitors
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (show MAPK1 Proteins)) is essential for drug-induced COX-2 (show PTGS2 Proteins) 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.
cyclophilin (show PPIA Proteins)-dependent isomerisation of p38MAPK is an important novel mechanism in regulating p38MAPK phosphorylation and functions.
MEK2 (show MAP2K2 Proteins) was essential for the phosphorylation of MKK3 (show MAP2K3 Proteins)/MKK6 (show MAP2K6 Proteins) and p38 MAPK that directly impacted on cyclin D1 (show CCND1 Proteins) expression.
stress-induced activation of p38 MAPK and apoptosis in endothelial cells and established the link between the acid sphingomyelinase (show SMPD1 Proteins)/ceramide and p38 MAPK pathways.
The results of this study suggest for the first time that cadmium induces MUC8 expression via TLR4 (show TLR4 Proteins)-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells
These data suggested that t-BHP induced both apoptosis and necroptosis in endothelial cells which was mediated by ROS (show ROS1 Proteins) and p38MAPK. ROS (show ROS1 Proteins) derived from NADPH oxidase (show NOX1 Proteins) and mitochondria contributed to t-BHPL and t-BHPH-induced apoptosis and necroptosis, respectively
TNF-alpha stimulated IL-33 expression through ERK, p38, and NFkappaB pathways in primary nasal epithelial cells and A549 cells
S. aureus evades phagophores and prevents further degradation by a MAPK14/p38alpha MAP kinase (show MAPK1 Proteins)-mediated blockade of autophagy.
p38 (show CRK Proteins)-dependent mechanism that phosphorylates GATA-2 (show GATA2 Proteins) and increases GATA-2 (show GATA2 Proteins) target gene activation has been demonstrated. This mechanism establishes a growth-promoting chemokine (show CCL1 Proteins)/cytokine circuit in acute myeloid leukemia (show BCL11A Proteins) cells.
our results strongly indicate that the crosstalk between p38 (show CRK Proteins) and Akt (show AKT1 Proteins) pathways can determine special AT-rich sequence-binding protein 2 (show SATB2 Proteins) expression and epithelial character of non-small-cell lung carcinoma cells
Osmotic stress promotes TEAD4 (show TEAD4 Proteins) cytoplasmic translocation via p38 MAPK in a Hippo-independent manner. Stress-induced TEAD inhibition predominates YAP (show YAP1 Proteins)-activating signals and selectively suppresses YAP (show YAP1 Proteins)-driven cancer cell growth.
cyclophilin (show PPIE Proteins)-dependent isomerisation of p38MAPK is an important novel mechanism in regulating p38MAPK phosphorylation and functions.
findings identify p38alpha MAPK (show MAPK1 Proteins) as a key component of PTH (show PTH Proteins) 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 (show TRPV1 Proteins), through genetic deletion or systemic or intra-nucleus accumbens (NAc) 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 p38 MAPK or TRPV1 (show TRPV1 Proteins) dampened protein expression levels of p-p38 MAPK, AC1 (show HRASLS Proteins), and p-NF-kappaB (show NFKB1 Proteins) which are normally induced by morphine ...
Results demonstrate that in vivo attenuation of p38alpha activity slows age-associated decline in dentate gyrus neurogenesis and associated cognitive function. Aged DN-p38alphaAF/+ mice produce more adult-born neurons than wildtype littermates, suggesting that p38alpha negatively contributes to age-dependent decline in neurogenesis that underlies the age-dependent decline in context discrimination.
bn1 (show CCR6 Proteins) expression is induced during myoblast differentiation, in a p38 MAP kinase- and MyoD (show MYOD1 Proteins)- dependent manner. RNAi-mediated depletion of drebrin (show DBN1 Proteins), or treatment with a chemical drebrin (show DBN1 Proteins) inhibitor, resulted in a similar phenotype in myoblasts: defective differentiation, with low levels of early and late differentiation markers and inefficient production of myofibers.
In vitro, SCF (show KITLG Proteins) induced the phosphorylation of p38 MAPK and cofilin (show CFL1 Proteins), leading to the migration of cardiac stem cells.
Park2 (show PARK2 Proteins) deficiency exacerbates ethanol-induced dopaminergic neuron damage through p38 (show CRK Proteins) kinase dependent inhibition of autophagy and mitochondrial function.
Mechanistic experiments revealed that treatment with cryptotanshinone activated AMPKalpha (show GRK4 Proteins) and p38-MAPK via their phosphorylation: the two major signaling pathways regulating energy metabolism.
This is the first report proclaiming that the ESAT-6 regulates Prdx-1 (show PRDX1 Proteins) which is involved in the increase of mycobacterial uptake and survival. The intermediate mechanisms involve the increased Prdx-1 (show PRDX1 Proteins) production in macrophages through the activation of p38 (show CRK Proteins) and NRF-2 (show NFE2L2 Proteins) dependent signaling.
These findings suggest that the TQ-induced production of ROS (show ROS1 Proteins) causes dedifferentiation through the ERK (show MAPK1 Proteins) 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 Proteins), p53 (show TP53 Proteins) and caspase-3 (show CASP3 Proteins) activation.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (show IL10 Proteins) production through p38 MAPK activation.
JNK (show MAPK8 Proteins) 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 (show CYCS Proteins) microinjection induces p38 phosphorylation through caspase-3 (show CASP3 Proteins) activation, and caspase (show CASP3 Proteins) 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