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anti-Human p38 Anticorps:
anti-Rat (Rattus) p38 Anticorps:
anti-Mouse (Murine) p38 Anticorps:
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Human Polyclonal p38 Primary Antibody pour IHC, WB - ABIN6714309
Li, He, Feng, Zhang, Tang, Bian, Bai, Zhou, Jiang, Heximer, Qin, Huang, Liu, Huang: Regulator of G protein signaling 5 protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload. dans Proceedings of the National Academy of Sciences of the United States of America 2010
Show all 21 Pubmed References
Human Polyclonal p38 Primary Antibody pour IHC, WB - ABIN6711591
Xu, Zheng, Xu, Yin, Qi, Xu, Han, Peng: Protective effects of dioscin against alcohol-induced liver injury. dans Archives of toxicology 2015
Show all 18 Pubmed References
Human Polyclonal p38 Primary Antibody pour IF (cc), IF (p) - ABIN671241
Li, Dong, Song, Xu, Liu, Song: Nrf2/ARE pathway activation, HO-1 and NQO1 induction by polychlorinated biphenyl quinone is associated with reactive oxygen species and PI3K/AKT signaling. dans Chemico-biological interactions 2014
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Human Polyclonal p38 Primary Antibody pour IF (p), IHC (p) - ABIN710141
Zhao, Liu, Liu, Han, Zhao: Betulin attenuates lung and liver injuries in sepsis. dans International immunopharmacology 2015
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Human Polyclonal p38 Primary Antibody pour IHC, WB - ABIN6713301
Qin, Zhu, Ji, Chunmei-Shi, Kou, Zhu, Zhang, Wang, Ni, Guo: Monoclonal antibody to six transmembrane epithelial antigen of prostate-4 influences insulin sensitivity by attenuating phosphorylation of P13K (P85) and Akt: possible mitochondrial mechanism. dans Journal of bioenergetics and biomembranes 2011
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Human Polyclonal p38 Primary Antibody pour IF, IHC - ABIN6713300
Xiao, Moon, Yan, Nian, Zhang, Liu, Lu, Guan, Chen, Jiang, Jiang, Liu, Li: Cellular FLICE-inhibitory protein protects against cardiac remodelling after myocardial infarction. dans Basic research in cardiology 2012
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Human Polyclonal p38 Primary Antibody pour ELISA, ICC - ABIN6267706
Liu, Zheng, Zhang, Wang, Yang, Bai, Dai: Fucoxanthin Activates Apoptosis via Inhibition of PI3K/Akt/mTOR Pathway and Suppresses Invasion and Migration by Restriction of p38-MMP-2/9 Pathway in Human Glioblastoma Cells. dans Neurochemical research 2017
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Human Polyclonal p38 Primary Antibody pour IHC, IHC (p) - ABIN152964
Ito, Miyado, Nakagawa, Muraki, Imai, Yamakawa, Qin, Hosoi, Saito, Takahashi: Age-associated changes in the subcellular localization of phosphorylated p38 MAPK in human granulosa cells. dans Molecular human reproduction 2010
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Human Polyclonal p38 Primary Antibody pour ELISA, ICC - ABIN6263958
Zou, Xiang, Wang, Peng, Wei: Oregano Essential Oil Improves Intestinal Morphology and Expression of Tight Junction Proteins Associated with Modulation of Selected Intestinal Bacteria and Immune Status in a Pig Model. dans BioMed research international 2017
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Human Monoclonal p38 Primary Antibody pour ICS - ABIN1177122
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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Deletion of p38alphaMAPK in microglia only, was sufficient to attenuate inflammatory responses following traumatic brain injury.
Based on the experimentally determined models and parameters, dynamics of the p38alpha-MKK6-MKP5 system were explored, demonstrating for the first time that bistability can arise with this model at biologically feasible parameter values
Aryl hydrocarbon receptor activation does not mediate skatole-induced ERK, p38 and JNK activation in intestinal epithelial cells.
Findings indicate that oxidative stress-triggered phosphorylation of p38alpha significantly enhances17,20- lyase activity with relatively constant 17alpha-hydroxylase activity, leading to overproduction of DHEA. This process may be a common mechanism that contributes to the hyperandrogenic state.
we discovered that TGF-b1 induces phosphorylation of JNK, p38, and Erk, whereas the activation of these kinases was reversed by dioscin treatment in a dose-dependent manner. . these data indicated that dioscin inhibits EMT in HepG2 cells, which is mediated in large part by inhibition of the p38-MAPK signaling
VSMC-MAPK14 is required for injury-induced neointima formation, likely through suppressing VSMC differentiation and promoting VSMC proliferation and inflammation. Our study will provide mechanistic insights into therapeutic strategies for mitigation of vascular stenosis.
Ablation of DeltaNp63 alpha leads to cell cycle arrest and growth retardation, due to, in part, upregulation of p38 MAPK phosphorylation and activation.
p38alpha destabilizes p63 to limit epidermal stem cell frequency and tumorigenic potential
The pharmaceutical inhibition with p38MAPK-specific inhibitor SCIO-469 revealed that p38MAPK-related signalling axis regulates ARID1A expression and thereby modulates paclitaxel sensitivity in triple-negative breast cancer triple-negative breast cancer (TNBC)
Study show that p38alpha regulates the acquisition of an endothelial-like phenotype by mesenchymal cells in colon tumors and damage tissue. Results indicate that p38alpha in mesenchymal cells restrains a TGF-beta-induced angiogenesis program including their ability to transdifferentiate into endothelial cells.
mismatch repair-deficient (dMMR)-competent stage III tumours harbouring BRAF mutations have an improved prognosis when strong nuclear phosphorylation of both ERK and p38MAPK is present.
Ngb promotes axon regeneration via oxygen-Ngb-p38-GAP43 signaling during ischemia/reperfusion.
It is a serine/threonine-specific protein kinase that transduces intracellular signals in critical cellular phenomena.
Studied role of Physalin A as an antineoplastic agent in activation of nuclear factor erythroid 2 (Nrf2) and p38 pathway and subsequent increase in quinone reductase expression.
Cadmium promotes colon cancer cell migration through ROS-dependent activation of p38 MAPK.
The authors performed a large-scale small molecule screen and found that the p38 MAPK pathway is involved in coordinating cell size and cell cycle progression. Small cells display higher p38 activity and spend more time in G1 than larger cells.
The results of the present study demonstrated that EPDMNQ and ENDMNQ induced apoptosis through ROSmodulated MAPK and STAT3 signaling pathways in Hep3B cells. Therefore, these novel 1,4naphthoquinone derivatives may be useful as anticancer agents for the treatment of liver cancer.
Study identified p38alpha and p38delta as critical regulators of ASC oligomerization, inflammasome activation, and IL-1beta secretion in keratinocytes. Furthermore, data suggest that the nature of the mitogen-activated protein kinase regulating inflammasome activity exhibits a certain cell specificity, with p38 playing a predominant role in keratinocytes and Jun N-terminal kinase 1 in cells of myeloid origin.
These findings allowed us to develop an effective strategy to attenuate the negative polybrene impact on the hMESCs properties during lentiviral infection by inhibiting the activity of p38 MAPK.
These observations indicate that p38alpha probably blocks brown adipose tissue thermogenesis through p38delta inhibition.
results suggest that ET-1-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase-PKCalpha-p(38)MAPK and NFkappaB-MT1MMP signaling pathways along with a marked decrease in TIMP-2 expression in the cells
cross-talk between p(38)MAPK and Gialpha play a pivotal role for full activation of cPLA2 during ET-1 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 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 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 involves activation of p38 and JNK MAPKs
These data suggest a differential requirement of JNK1 and p38 MAPK in TNF regulation of E2F1. Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF-mediated EC dysfunction.
p38 MAPK (MAPK14) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.
involvement of p38 MAP kinase activities and caldesmon phosphorylation in the MLCK-independent regulation of thrombin-induced endothelial cell permeability.
involvement of p38 MAP kinase in the hyaluronan oligosaccharide induction of MMP-13
These data indicate that early transient activation of MAPK-p38 in bovine mononuclear phagocytes by Mycobacterium avium subsp. paratuberculosis (MAP) organisms may be a key to the capacity of MAP to survive in bovine monocytes.
Replacement of distention with pharmacological relaxation reduced the increase in p38 expression, but not extracellular signal-regulated kinases.
dynamic compression stimulates cell proliferation and proteoglycan synthesis in the presence of IL-1beta and/or inhibitors of the MAPKs and NFkappaB and AP-1 signalling pathways
results suggest that Nav1.7-Ca2+ influx-protein kinase C-alpha pathway activated ERK1/ERK2 and p38, which increased phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation
Thrombospondin 1, fibronectin, and vitronectin are differentially dependent upon RAS, ERK1/2, and p38 for induction of vascular smooth muscle cell chemotaxis.
findings indicate that cell-permeable p38 protein may be useful in preventing the degeneration of higher brain function occurring through hippocampal neuronal cell death.
Our findings suggest that erythropoietin gene modified mesenchymal stem cells (EPO-MSCs) maybe attenuate bronchopulmonary dysplasia (BPD) injury in early than in late administration by inhibiting inflammation response through down-regulation of the p38MAPK signalling pathway
Study using knock-in mouse model elucidated the role of the p38alpha-TAB1 interaction during myocardial ischemia in vivo suggested that persistent p38alpha activation may be the result of the disinhibition of MAP2K3 access in the absence of TAB1 docking on p38alpha and proposed that TAB1 phosphorylation downstream of p38alpha is associated with cardiac damage during ischemia.
data suggest that Caspase-3 inhibits chemical-induced hepatocarcinogenesis by suppressing p38 activation and hepatocyte death.
alpha-synucleinA53T overexpression caused p38 MAPK activation, then p38 MAPK directly phosphorylated Parkin at serine 131 to disrupt the Parkin's protective function.
data provide evidence for a tumour suppressor role of Trib2 in myeloid leukaemia via activation of p38 stress signalling. This newly identified role indicates that Trib2 may counteract the propagation and chemotherapy resistance of leukaemia cells.
neuronal p38alpha negatively regulates JNK activity that is required for specific modulation of anxiety-related behaviour.
These results demonstrate that high glucose induces C3 up-regulation via RAGE- p38MAPK-NF-kappaB signalling in vivo and in vitro, which might be associated with synaptic protein loss.
Using cell-type-specific gene deletion, study shows that astrocytic p38alpha MAPK is required for the increased astrocytic glutamate release and astrocyte-to-neuron communication during low-frequency stimulation. Accordingly, removal of astrocytic (but not neuronal) p38alpha abolishes long-term depression expression. Finally, this mechanism modulates long-term memory in vivo.
cisplatin activates TAK1, which phosphorylates p38 and ERK, leading to excessive autophagy of tubular epithelial cells that exacerbates kidney damage.
Findings identify mitogen-activated protein kinase 14 (p38alpha MAPK) as a regulator of muscle atrophy and suggest that the suppression of intracellular signaling mediated by p38alpha MAPK serves as a potential target for the treatment of muscle atrophy.
this study shows that p38alpha has an important role in antigen cross-presentation by dendritic cells
we investigated the p38 MAPK pathway and found that loss of Trio blocked the cascade transduction of p38 MAPK signaling. In conclusion, we identified Trio as a novel coordinator in regulating root development and clarified its relevant molecular events
The in vivo results revealed that DHL significantly attenuated LPS-induced pathological injury and reduced cytokines expression in the lung. NF-kappaB, p38 MAPK/MK2 and Akt signaling molecules were also involved in the anti-inflammatory effect.
These results indicate that natriuretic peptide exerts a renoprotective effect via inhibiting phosphorylation of p38 MAPK in podocytes.
High p38MAPK expression is associated with abdominal aortic aneurysm.
P38 and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
Adult zebrafish cardiomyocytes express active p38alpha MAPK, which is switched off upon entry into mitosis.
Dkk3r regulates p38a phosphorylation to maintain Smad4 stability, in turn enabling the Smad2.Smad3a.Smad4 complex to form and activate the myf5 promoter.
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.
Csaids binding protein
, MAP kinase 14
, MAP kinase 2
, MAP kinase Mxi2
, MAP kinase p38 alpha
, MAPK 14
, MAX-interacting protein 2
, cytokine suppressive anti-inflammatory drug binding protein
, cytokine-supressive anti-inflammatory drug binding protein
, mitogen-activated protein kinase 14
, mitogen-activated protein kinase 14A
, mitogen-activated protein kinase p38 alpha
, p38 MAP kinase
, p38 mitogen activated protein kinase
, p38alpha Exip
, reactive kinase
, stress-activated protein kinase 2A
, 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
, MAP kinase 14A
, MAP kinase p38a
, MAPK 14A
, Mitogen-activated protein kinase p38a
, mitogen-activated protein kinase p38a