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anti-Human MAPK14 Antikörper:
anti-Mouse (Murine) MAPK14 Antikörper:
anti-Rat (Rattus) MAPK14 Antikörper:
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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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Dog (Canine) Monoclonal MAPK14 Primary Antibody für 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 für 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 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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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
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.
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
Gab1/SHP2 (zeige PTPN11 Antikörper)/p38MAPK signaling pathway and Ang-2 (zeige ANGPT2 Antikörper) have an essential role in regulating thrombin (zeige F2 Antikörper)-induced monocyte adhesion and vascular leakage
Studies suugest Wip1 (zeige PPM1D Antikörper) role in tumorigenesis through regulation of p53 (zeige TP53 Antikörper) and p38MAPK pathways.
p38 (zeige CRK Antikörper) role in the Helicobacter pylori podocyte infiltration
Our data suggest that rCC16 suppresses LPS (zeige TLR4 Antikörper)-mediated inflammatory mediator TNF-alpha (zeige TNF Antikörper), IL-6 (zeige IL6 Antikörper), and IL-8 (zeige IL8 Antikörper) production by inactivating NF-kappaB (zeige NFKB1 Antikörper) and p38 MAPK but not AP-1 (zeige JUN Antikörper) 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 (zeige BCL10 Antikörper)/CARD9 (zeige CARD9 Antikörper)/p38 MAPK signalling. Zinc supplement ameliorates ORCH through activation of metallothionein (zeige MT Antikörper) to repress oxidative stress-activated BCL10 (zeige BCL10 Antikörper) expression and p38 MAPK activation.
involvement of CacyBP/SIP (zeige CACYBP Antikörper) in the regulation of p38 (zeige CRK Antikörper) kinase activity, in addition to that of ERK1/2, might point to the function of CacyBP/SIP (zeige CACYBP Antikörper) in pro-survival and pro-apoptotic pathways.
Macrophage p38alpha-deficient mice had decreased mortality and GalN (zeige GAL Antikörper)/TNF-alpha (zeige TNF Antikörper)-induced liver injury apoptosis, less apoptosis, accelerated regeneration, decreased granulocyte recruitment, monocytes infiltration, and cytokine production after GalN (zeige GAL Antikörper)/TNF-alpha (zeige TNF Antikörper) treatment. Mechanistically, p38 (zeige CRK Antikörper) signaling was activated by lipopolysaccharide/interferon-gamma (zeige IFNG Antikörper) treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibi
results suggest that the TLR2-p38 (zeige CRK Antikörper)-CD86 (zeige CD86 Antikörper) signaling pathway plays a vital role in inflammation associated with burn injury
Overall, our results provide the first evidence that HDAC6 (zeige HDAC6 Antikörper) is capable of inducing expression of pro-inflammatory genes by regulating the ROS (zeige ROS1 Antikörper)-MAPK (zeige MAPK1 Antikörper)-NF-kappaB (zeige NFKB1 Antikörper)/AP-1 (zeige JUN Antikörper) 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 (zeige NFE2L2 Antikörper)) that up-regulated heme oxygenase-1 (HO-1 (zeige HMOX1 Antikörper)) expression in addition to other genes.
Trehalose may rescue against insulin (zeige INS Antikörper) resistance-induced myocardial contractile defect and apoptosis, via autophagy associated with dephosphorylation of p38 MAPK and Foxo1 (zeige FOXO1 Antikörper) without affecting phosphorylation of Akt (zeige AKT1 Antikörper).
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.
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.
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
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