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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.
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.
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.
TGF-beta (show TGFB1 Proteins) induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]), which in turn phosphorylates NR4A1 (show NR4A1 Proteins), resulting in nuclear export of the receptor.
Data suggest that suppression of nonsense-mediated RNA decay due to persistent DNA damage (from exposure to either mutagens, gamma rays, or oxidative stress) requires the activity of p38alpha MAPK (show MAPK1 Proteins) (MAPK14, mitogen-activated protein kinase 14, MAP kinase p38 alpha); mRNA of ATF3 (activating transcription factor 3 (show ATF3 Proteins)) is stabilized by persistent DNA damage in a p38alpha MAPK (show MAPK1 Proteins)-dependent manner.
VEGF (show VEGFA Proteins)-activated p38alpha phosphorylates coronin 1B (show CORO1B Proteins) at Ser2 (show JAG2 Proteins) and activates the Arp2 (show ACTR2 Proteins)/3 complex by liberating it from coronin 1B (show CORO1B Proteins).
findings show that endothelial MAPKs ERK (show EPHB2 Proteins), p38 (show CRK Proteins), and JNK (show MAPK8 Proteins) mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 (show ICAM1 Proteins) in cerebral and dermal microvascular endothelial cells
Tetraarsenic hexoxide (As4O6) induced G2/M arrest, apoptosis and autophagic cell death through PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) and p38 MAPK pathways alteration in SW620 colon cancer cells.
The N-Terminal phosphorylation of RB by p38 (show CRK Proteins) bypasses its inactivation by cyclin (show PCNA Proteins)-dependent kinases and prevents proliferation in cancer cells.
Inhibition of MAPK14 conclusively facilitates elucidation of the impact of the complex network of p38 MAPK signaling on atherogenesis.
Collectively, this study provides more insights into RELT (show RELT Proteins) expression, RELT (show RELT Proteins) family member function, and the mechanism of RELT (show RELT Proteins)-induced death.
Data suggest that Mapk14/p38alpha is activated and forms cystine disulfide-bound heterodimer with Map2k3/Mkk3 (show MAP2K3 Proteins) in cardiomyocytes and isolated hearts during oxidative stress. (Mapk14, mitogen-activated protein kinase 14; Mkk3 (show MAP2K3 Proteins) = mitogen-activated protein kinase kinase 3 (show MAP2K3 Proteins))
High-glucose induces tau hyperphosphorylation through activation of TLR9 (show TLR9 Proteins)-P38 MAPK pathway.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (show ROS1 Proteins)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (show TP53 Proteins), p38 (show CRK Proteins) and JNK (show MAPK8 Proteins) MAPKs, culminating in an increase in autophagy and apoptosis markers.
Soluble epoxide hydrolase (show EPHX2 Proteins) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (show CRK Proteins)/Smad3 (show SMAD3 Proteins) signaling pathway.
These results provide evidence supporting a key role for the p38 MAPK signaling pathway which is involved in the regulation of Abeta1-42 internalization in the parietal cortex and hippocampus of mouse through LRP1 (show LRP1 Proteins) in vivo.
Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the mRNA and protein expressions of p-p38MAPK, AAT (show SERPINA1A Proteins), signal transducer and activator of transcription 1 (STAT1 (show STAT1 Proteins)) and activating transcription factor2 (ATF2 (show ATF2 Proteins))
p38alpha is essential to maintain in actin dynamics with age in hepatocytes.
Data, including data from studies conducted in cells from transgenic/knockout mice, suggest that p38alpha MAPK (show MAPK1 Proteins) (Mapk14) activity is required for hypoxia-induced pro-angiogenic activity involving cardiomyocytes and vascular endothelial cells; p38 MAPK activation in cardiomyocyte is sufficient to promote paracrine signaling-mediated, pro-angiogenic activity/myocardial revascularization.
blockage of NF-kappaB (show NFKB1 Proteins) p65 (show NFkBP65 Proteins) and/or MAPK p38 (show MAPK1 Proteins) with their specific inhibitors strongly attenuated B7-H3 (show CD276 Proteins)-amplified inflammatory response with significantly reduced proinflammatory cytokine and chemokine (show CCL1 Proteins) production, and markedly ameliorated B7-H3 (show CD276 Proteins)-exacerbated disruption of blood-brain barrier and severity of disease status in S. pneumoniae-infected mice.
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