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results suggest that ET-1 (Montrer EDN1 Kits ELISA)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (Montrer NOX1 Kits ELISA)-PKCalpha (Montrer PKCa Kits ELISA)-p(38)MAPK (Montrer MAPK1 Kits ELISA) and NFkappaB-MT1MMP (Montrer MMP14 Kits ELISA) signaling pathways along with a marked decrease in TIMP-2 (Montrer TIMP2 Kits ELISA) expression in the cells
cross-talk between p(38)MAPK (Montrer MAPK1 Kits ELISA) and Gialpha play a pivotal role for full activation of cPLA2 (Montrer PLA2G4A Kits ELISA) during ET-1 (Montrer EDN1 Kits ELISA) 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 (Montrer MMP13 Kits ELISA) 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 (Montrer MAPK8 Kits ELISA) 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 Kits ELISA) involves activation of p38 and JNK (Montrer MAPK8 Kits ELISA) MAPKs
These data suggest a differential requirement of JNK1 (Montrer MAPK8 Kits ELISA) and p38 MAPK in TNF (Montrer TNF Kits ELISA) regulation of E2F1 (Montrer E2F1 Kits ELISA). Targeted inactivation of JNK1 (Montrer MAPK8 Kits ELISA) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (Montrer TNF Kits ELISA)-mediated EC dysfunction.
p38 MAPK (MAPK14) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.
ROS (Montrer ROS1 Kits ELISA)/JNK (Montrer MAPK8 Kits ELISA)/p38/Upd (Montrer UROD Kits ELISA) 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 (Montrer MAPK1 Kits ELISA) and Rack1 (Montrer GNB2L1 Kits ELISA) 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 (Montrer MAPK1 Kits ELISA) 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 (Montrer MAPK1 Kits ELISA) 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 pathway and DREF is involved in the regulation of proliferation and differentiation of Drosophila ISCs (Montrer NFS1 Kits ELISA) and progenitors
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (Montrer MAPK1 Kits ELISA)) is essential for drug-induced COX-2 (Montrer PTGS2 Kits ELISA) 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.
S. aureus evades phagophores and prevents further degradation by a MAPK14/p38alpha MAP kinase (Montrer MAPK1 Kits ELISA)-mediated blockade of autophagy.
p38 (Montrer CRK Kits ELISA)-dependent mechanism that phosphorylates GATA-2 (Montrer GATA2 Kits ELISA) and increases GATA-2 (Montrer GATA2 Kits ELISA) target gene activation has been demonstrated. This mechanism establishes a growth-promoting chemokine (Montrer CCL1 Kits ELISA)/cytokine circuit in acute myeloid leukemia (Montrer BCL11A Kits ELISA) cells.
our results strongly indicate that the crosstalk between p38 (Montrer CRK Kits ELISA) and Akt (Montrer AKT1 Kits ELISA) pathways can determine special AT-rich sequence-binding protein 2 (Montrer SATB2 Kits ELISA) expression and epithelial character of non-small-cell lung carcinoma cells
Osmotic stress promotes TEAD4 (Montrer TEAD4 Kits ELISA) cytoplasmic translocation via p38 MAPK in a Hippo-independent manner. Stress-induced TEAD inhibition predominates YAP (Montrer YAP1 Kits ELISA)-activating signals and selectively suppresses YAP (Montrer YAP1 Kits ELISA)-driven cancer cell growth.
TGF-beta (Montrer TGFB1 Kits ELISA) induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]), which in turn phosphorylates NR4A1 (Montrer NR4A1 Kits ELISA), 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 (Montrer MAPK1 Kits ELISA) (MAPK14, mitogen-activated protein kinase 14, MAP kinase p38 alpha); mRNA of ATF3 (activating transcription factor 3 (Montrer ATF3 Kits ELISA)) is stabilized by persistent DNA damage in a p38alpha MAPK (Montrer MAPK1 Kits ELISA)-dependent manner.
VEGF (Montrer VEGFA Kits ELISA)-activated p38alpha phosphorylates coronin 1B (Montrer CORO1B Kits ELISA) at Ser2 (Montrer JAG2 Kits ELISA) and activates the Arp2 (Montrer ACTR2 Kits ELISA)/3 complex by liberating it from coronin 1B (Montrer CORO1B Kits ELISA).
findings show that endothelial MAPKs ERK (Montrer EPHB2 Kits ELISA), p38 (Montrer CRK Kits ELISA), and JNK (Montrer MAPK8 Kits ELISA) mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 (Montrer ICAM1 Kits ELISA) in cerebral and dermal microvascular endothelial cells
Tetraarsenic hexoxide (As4O6) induced G2/M arrest, apoptosis and autophagic cell death through PI3K (Montrer PIK3CA Kits ELISA)/Akt (Montrer AKT1 Kits ELISA) and p38 MAPK pathways alteration in SW620 colon cancer cells.
The N-Terminal phosphorylation of RB by p38 (Montrer CRK Kits ELISA) bypasses its inactivation by cyclin (Montrer PCNA Kits ELISA)-dependent kinases and prevents proliferation in cancer cells.
P38 MAPK-mediated YAP (Montrer YAP1 Kits ELISA) activation controls mechanical-tension-induced pulmonary alveolar regeneration.
The anti-inflammatory functions of p38 MAPK in macrophages are critically dependent on production of IL-10 (Montrer IL10 Kits ELISA).
this study shows that peripheral deletion of CD8 (Montrer CD8A Kits ELISA) T cells requires p38 MAPK in cross-presenting dendritic cells
Distal retinal ganglion cell axon transport loss and activation of p38 MAPK stress pathway following VEGF-A (Montrer VEGFA Kits ELISA) antagonism have been documented.
p38MAPK/MK2 (Montrer KCNA2 Kits ELISA) phosphorylation of RIPK1 (Montrer RIPK1 Kits ELISA) is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.
Data suggest that Mapk14/p38alpha is activated and forms cystine disulfide-bound heterodimer with Map2k3/Mkk3 (Montrer MAP2K3 Kits ELISA) in cardiomyocytes and isolated hearts during oxidative stress. (Mapk14, mitogen-activated protein kinase 14; Mkk3 (Montrer MAP2K3 Kits ELISA) = mitogen-activated protein kinase kinase 3 (Montrer MAP2K3 Kits ELISA))
High-glucose induces tau hyperphosphorylation through activation of TLR9 (Montrer TLR9 Kits ELISA)-P38 MAPK pathway.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (Montrer ROS1 Kits ELISA)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (Montrer TP53 Kits ELISA), p38 (Montrer CRK Kits ELISA) and JNK (Montrer MAPK8 Kits ELISA) MAPKs, culminating in an increase in autophagy and apoptosis markers.
Soluble epoxide hydrolase (Montrer EPHX2 Kits ELISA) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (Montrer CRK Kits ELISA)/Smad3 (Montrer SMAD3 Kits ELISA) signaling pathway.
These findings suggest that the TQ-induced production of ROS (Montrer ROS1 Kits ELISA) causes dedifferentiation through the ERK (Montrer MAPK1 Kits ELISA) 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 (Montrer NFKB1 Kits ELISA), p53 (Montrer TP53 Kits ELISA) and caspase-3 (Montrer CASP3 Kits ELISA) activation.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (Montrer IL10 Kits ELISA) production through p38 MAPK activation.
JNK (Montrer MAPK8 Kits ELISA) 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 (Montrer MAPK1/3 Kits ELISA), in the neuroretina and retinal arteries.
cytochrome c (Montrer CYCS Kits ELISA) microinjection induces p38 phosphorylation through caspase-3 (Montrer CASP3 Kits ELISA) activation, and caspase (Montrer CASP3 Kits ELISA) 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