Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human p38 Anticorps:
anti-Rat (Rattus) p38 Anticorps:
anti-Mouse (Murine) p38 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
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
Show all 12 Pubmed References
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
Show all 6 Pubmed References
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
Show all 5 Pubmed References
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
Show all 4 Pubmed References
Human Monoclonal p38 Primary Antibody pour FACS, IF - ABIN968799
Han, Lee, Bibbs, Ulevitch: A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. dans Science (New York, N.Y.) 1994
Show all 3 Pubmed References
Human Monoclonal p38 Primary Antibody pour FACS, IF - ABIN968800
Winston, Chan, Johnson, Riches: Activation of p38mapk, MKK3, and MKK4 by TNF-alpha in mouse bone marrow-derived macrophages. dans Journal of immunology (Baltimore, Md. : 1950) 1997
Show all 3 Pubmed References
Overall, these results suggest that p53 (Montrer TP53 Anticorps) is involved in improving insulin (Montrer INS Anticorps) sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB (Montrer NFKB1 Anticorps) pathways.
Data show that the combination of targeting RAD51 (Montrer RAD51 Anticorps) and p38 (Montrer CRK Anticorps) inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1 (Montrer PARP1 Anticorps).
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 (Montrer CRK Anticorps)-p38IP (Montrer SUPT20H Anticorps) is required for the Snail (Montrer SNAI1 Anticorps)-induced E-cadherin (Montrer CDH1 Anticorps) down-regulation and cell invasion in HNSCC
GATA4 (Montrer GATA4 Anticorps) is a regulator of osteoblastic differentiation via the p38 (Montrer CRK Anticorps) signaling pathways.
CX3CL1 (Montrer CX3CL1 Anticorps)/CX3CR1 (Montrer CX3CR1 Anticorps) axis plays a key role in the development of ischemia-induced oligodendrocyte injury via p38MAPK (Montrer MAPK14 Anticorps) signaling pathway.
Data suggest that in vitro-induction of CD8 (Montrer CD8A Anticorps)+ Tregs depended in part on transforming growth factor beta 1 (TGF-beta1 (Montrer TGFB1 Anticorps)) activation of p38 MAPK (Montrer MAPK14 Anticorps) signaling, and that p38 MAPK (Montrer MAPK14 Anticorps) could be a therapeutic target in ovarian cancer (OC) anti-tumor immunotherapy.
present study provides evidence that variations in GADD45B (Montrer GADD45B Anticorps) rs2024144T, MAPK14 (Montrer MAPK14 Anticorps) rs3804451A and GADD45A (Montrer GADD45A Anticorps) rs581000C may predict platinum-based chemotherapy toxicity outcomes in patients with advanced non-small cell lung cancer
Gab1/SHP2 (Montrer PTPN11 Anticorps)/p38MAPK (Montrer MAPK14 Anticorps) signaling pathway and Ang-2 (Montrer ANGPT2 Anticorps) have an essential role in regulating thrombin (Montrer F2 Anticorps)-induced monocyte adhesion and vascular leakage
Studies suugest Wip1 (Montrer PPM1D Anticorps) role in tumorigenesis through regulation of p53 (Montrer TP53 Anticorps) and p38MAPK (Montrer MAPK14 Anticorps) pathways.
results suggest that ET-1 (Montrer EDN1 Anticorps)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (Montrer NOX1 Anticorps)-PKCalpha (Montrer PKCa Anticorps)-p(38)MAPK (Montrer MAPK1 Anticorps) and NFkappaB-MT1MMP (Montrer MMP14 Anticorps) signaling pathways along with a marked decrease in TIMP-2 (Montrer TIMP2 Anticorps) expression in the cells
cross-talk between p(38)MAPK (Montrer MAPK1 Anticorps) and Gialpha play a pivotal role for full activation of cPLA2 (Montrer PLA2G4A Anticorps) during ET-1 (Montrer EDN1 Anticorps) stimulation of pulmonary artery smooth muscle cells.
MAPK14 (Montrer MAPK14 Anticorps) signalling pathway is largely involved in heat-induced sperm damage.
p38 MAPK (Montrer MAPK14 Anticorps) is an early redox sensor in the laminar shear stress with hydrogen peroxide being a signaling mediator.
Blockade of p38 (Montrer MAPK14 Anticorps) enhances chondrocyte phenotype in monolayer culture and may promote more efficient cartilage tissue regeneration for cell-based therapies.
p38 (Montrer MAPK14 Anticorps) phosphorylation and MMP13 (Montrer MMP13 Anticorps) 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 (Montrer MAPK14 Anticorps) and JNK (Montrer MAPK8 Anticorps) 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 (Montrer SLC12A1 Anticorps) involves activation of p38 (Montrer MAPK14 Anticorps) and JNK (Montrer MAPK8 Anticorps) MAPKs
These data suggest a differential requirement of JNK1 (Montrer MAPK8 Anticorps) and p38 MAPK (Montrer MAPK14 Anticorps) in TNF (Montrer TNF Anticorps) regulation of E2F1 (Montrer E2F1 Anticorps). Targeted inactivation of JNK1 (Montrer MAPK8 Anticorps) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (Montrer TNF Anticorps)-mediated EC dysfunction.
p38 MAPK (MAPK14 (Montrer MAPK14 Anticorps)) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.
p38 (Montrer CRK Anticorps) role in the Helicobacter pylori podocyte infiltration
Our data suggest that rCC16 suppresses LPS (Montrer TLR4 Anticorps)-mediated inflammatory mediator TNF-alpha (Montrer TNF Anticorps), IL-6 (Montrer IL6 Anticorps), and IL-8 (Montrer IL8 Anticorps) production by inactivating NF-kappaB (Montrer NFKB1 Anticorps) and p38 MAPK (Montrer MAPK14 Anticorps) but not AP-1 (Montrer JUN Anticorps) 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 (Montrer BCL10 Anticorps)/CARD9 (Montrer CARD9 Anticorps)/p38 MAPK (Montrer MAPK14 Anticorps) signalling. Zinc supplement ameliorates ORCH through activation of metallothionein (Montrer MT Anticorps) to repress oxidative stress-activated BCL10 (Montrer BCL10 Anticorps) expression and p38 MAPK (Montrer MAPK14 Anticorps) activation.
involvement of CacyBP/SIP (Montrer CACYBP Anticorps) in the regulation of p38 (Montrer CRK Anticorps) kinase activity, in addition to that of ERK1/2, might point to the function of CacyBP/SIP (Montrer CACYBP Anticorps) in pro-survival and pro-apoptotic pathways.
Macrophage p38alpha (Montrer MAPK14 Anticorps)-deficient mice had decreased mortality and GalN (Montrer GAL Anticorps)/TNF-alpha (Montrer TNF Anticorps)-induced liver injury apoptosis, less apoptosis, accelerated regeneration, decreased granulocyte recruitment, monocytes infiltration, and cytokine production after GalN (Montrer GAL Anticorps)/TNF-alpha (Montrer TNF Anticorps) treatment. Mechanistically, p38 (Montrer CRK Anticorps) signaling was activated by lipopolysaccharide/interferon-gamma (Montrer IFNG Anticorps) treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibi
results suggest that the TLR2-p38 (Montrer CRK Anticorps)-CD86 (Montrer CD86 Anticorps) signaling pathway plays a vital role in inflammation associated with burn injury
Overall, our results provide the first evidence that HDAC6 (Montrer HDAC6 Anticorps) is capable of inducing expression of pro-inflammatory genes by regulating the ROS (Montrer ROS1 Anticorps)-MAPK (Montrer MAPK1 Anticorps)-NF-kappaB (Montrer NFKB1 Anticorps)/AP-1 (Montrer JUN Anticorps) pathways and serves as a molecular target for inflammation.
YZH-106 induced p38 MAPK (Montrer MAPK14 Anticorps) and ERK1/2 phosphorylation, which led to the activation of erythroid 2-related factor 2 (Nrf2 (Montrer NFE2L2 Anticorps)) that up-regulated heme oxygenase-1 (HO-1 (Montrer HMOX1 Anticorps)) expression in addition to other genes.
Trehalose may rescue against insulin (Montrer INS Anticorps) resistance-induced myocardial contractile defect and apoptosis, via autophagy associated with dephosphorylation of p38 MAPK (Montrer MAPK14 Anticorps) and Foxo1 (Montrer FOXO1 Anticorps) without affecting phosphorylation of Akt (Montrer AKT1 Anticorps).
P38 (Montrer MAPK14 Anticorps) and JNK (Montrer MAPK8 Anticorps) have opposing effects on persistence of in vivo leukocyte migration in zebrafish.
Adult zebrafish cardiomyocytes express active p38alpha (Montrer MAPK14 Anticorps) MAPK (Montrer MAPK1 Anticorps), which is switched off upon entry into mitosis.
Dkk3r regulates p38a (Montrer MAPK14 Anticorps) phosphorylation to maintain Smad4 (Montrer SMAD4 Anticorps) stability, in turn enabling the Smad2 (Montrer SMAD2 Anticorps).Smad3a.Smad4 complex to form and activate the myf5 (Montrer MYF5 Anticorps) 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
, CRK proto-oncogene, adaptor protein
, Proto-oncogene c-Crk
, adapter molecule crk
, proto-oncogene C-crk
, v-crk avian sarcoma virus CT10 oncogene homolog
, v-crk sarcoma virus CT10 oncogene homolog