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results suggest that ET-1 (显示 EDN1 ELISA试剂盒)-induced activation of proMMP-2 is mediated via cross-talk between NADPH oxidase (显示 NOX1 ELISA试剂盒)-PKCalpha (显示 PKCa ELISA试剂盒)-p(38)MAPK (显示 MAPK1 ELISA试剂盒) and NFkappaB-MT1MMP (显示 MMP14 ELISA试剂盒) signaling pathways along with a marked decrease in TIMP-2 (显示 TIMP2 ELISA试剂盒) expression in the cells
cross-talk between p(38)MAPK (显示 MAPK1 ELISA试剂盒) and Gialpha play a pivotal role for full activation of cPLA2 (显示 PLA2G4A ELISA试剂盒) during ET-1 (显示 EDN1 ELISA试剂盒) 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 (显示 MMP13 ELISA试剂盒) 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 (显示 MAPK8 ELISA试剂盒) 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 (显示 SLC12A1 ELISA试剂盒) involves activation of p38 and JNK (显示 MAPK8 ELISA试剂盒) MAPKs
These data suggest a differential requirement of JNK1 (显示 MAPK8 ELISA试剂盒) and p38 MAPK in TNF (显示 TNF ELISA试剂盒) regulation of E2F1 (显示 E2F1 ELISA试剂盒). Targeted inactivation of JNK1 (显示 MAPK8 ELISA试剂盒) at arterial injury sites may represent a potential therapeutic intervention for ameliorating TNF (显示 TNF ELISA试剂盒)-mediated EC dysfunction.
p38 MAPK (MAPK14) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.
ROS (显示 ROS1 ELISA试剂盒)/JNK (显示 MAPK8 ELISA试剂盒)/p38/Upd (显示 UROD ELISA试剂盒) 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 (显示 MAPK1 ELISA试剂盒) and Rack1 (显示 GNB2L1 ELISA试剂盒) 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 (显示 MAPK1 ELISA试剂盒) 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 (显示 MAPK1 ELISA试剂盒) 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 (显示 NFS1 ELISA试剂盒) and progenitors
p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.
p38 Mitogen-activated protein kinase (MAPK (显示 MAPK1 ELISA试剂盒)) is essential for drug-induced COX-2 (显示 PTGS2 ELISA试剂盒) 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 (显示 MAPK1 ELISA试剂盒)-mediated blockade of autophagy.
p38 (显示 CRK ELISA试剂盒)-dependent mechanism that phosphorylates GATA-2 (显示 GATA2 ELISA试剂盒) and increases GATA-2 (显示 GATA2 ELISA试剂盒) target gene activation has been demonstrated. This mechanism establishes a growth-promoting chemokine (显示 CCL1 ELISA试剂盒)/cytokine circuit in acute myeloid leukemia (显示 BCL11A ELISA试剂盒) cells.
our results strongly indicate that the crosstalk between p38 (显示 CRK ELISA试剂盒) and Akt (显示 AKT1 ELISA试剂盒) pathways can determine special AT-rich sequence-binding protein 2 (显示 SATB2 ELISA试剂盒) expression and epithelial character of non-small-cell lung carcinoma cells
Osmotic stress promotes TEAD4 (显示 TEAD4 ELISA试剂盒) cytoplasmic translocation via p38 MAPK in a Hippo-independent manner. Stress-induced TEAD inhibition predominates YAP (显示 YAP1 ELISA试剂盒)-activating signals and selectively suppresses YAP (显示 YAP1 ELISA试剂盒)-driven cancer cell growth.
TGF-beta (显示 TGFB1 ELISA试剂盒) induces p38alpha (mitogen-activated protein kinase 14 [MAPK14]), which in turn phosphorylates NR4A1 (显示 NR4A1 ELISA试剂盒), 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 (显示 MAPK1 ELISA试剂盒) (MAPK14, mitogen-activated protein kinase 14, MAP kinase p38 alpha); mRNA of ATF3 (activating transcription factor 3 (显示 ATF3 ELISA试剂盒)) is stabilized by persistent DNA damage in a p38alpha MAPK (显示 MAPK1 ELISA试剂盒)-dependent manner.
VEGF (显示 VEGFA ELISA试剂盒)-activated p38alpha phosphorylates coronin 1B (显示 CORO1B ELISA试剂盒) at Ser2 (显示 JAG2 ELISA试剂盒) and activates the Arp2 (显示 ACTR2 ELISA试剂盒)/3 complex by liberating it from coronin 1B (显示 CORO1B ELISA试剂盒).
findings show that endothelial MAPKs ERK (显示 EPHB2 ELISA试剂盒), p38 (显示 CRK ELISA试剂盒), and JNK (显示 MAPK8 ELISA试剂盒) mediate diapedesis-related and diapedesis-unrelated functions of ICAM-1 (显示 ICAM1 ELISA试剂盒) in cerebral and dermal microvascular endothelial cells
Tetraarsenic hexoxide (As4O6) induced G2/M arrest, apoptosis and autophagic cell death through PI3K (显示 PIK3CA ELISA试剂盒)/Akt (显示 AKT1 ELISA试剂盒) and p38 MAPK pathways alteration in SW620 colon cancer cells.
The N-Terminal phosphorylation of RB by p38 (显示 CRK ELISA试剂盒) bypasses its inactivation by cyclin (显示 PCNA ELISA试剂盒)-dependent kinases and prevents proliferation in cancer cells.
P38 MAPK-mediated YAP (显示 YAP1 ELISA试剂盒) 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 (显示 IL10 ELISA试剂盒).
this study shows that peripheral deletion of CD8 (显示 CD8A ELISA试剂盒) 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 (显示 VEGFA ELISA试剂盒) antagonism have been documented.
p38MAPK/MK2 (显示 KCNA2 ELISA试剂盒) phosphorylation of RIPK1 (显示 RIPK1 ELISA试剂盒) 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 (显示 MAP2K3 ELISA试剂盒) in cardiomyocytes and isolated hearts during oxidative stress. (Mapk14, mitogen-activated protein kinase 14; Mkk3 (显示 MAP2K3 ELISA试剂盒) = mitogen-activated protein kinase kinase 3 (显示 MAP2K3 ELISA试剂盒))
High-glucose induces tau hyperphosphorylation through activation of TLR9 (显示 TLR9 ELISA试剂盒)-P38 MAPK pathway.
Doxorubicin (Dox)-administration to cardiomyocytes increased the levels of reactive oxygen species (ROS (显示 ROS1 ELISA试剂盒)) in a time-dependent manner that followed the activation of stress-induced proteins p53 (显示 TP53 ELISA试剂盒), p38 (显示 CRK ELISA试剂盒) and JNK (显示 MAPK8 ELISA试剂盒) MAPKs, culminating in an increase in autophagy and apoptosis markers.
Soluble epoxide hydrolase (显示 EPHX2 ELISA试剂盒) inhibitor AUDA decreases bleomycin-induced pulmonary toxicity in mice by inhibiting the p38 (显示 CRK ELISA试剂盒)/Smad3 (显示 SMAD3 ELISA试剂盒) signaling pathway.
These findings suggest that the TQ-induced production of ROS (显示 ROS1 ELISA试剂盒) causes dedifferentiation through the ERK (显示 MAPK1 ELISA试剂盒) 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 (显示 NFKB1 ELISA试剂盒), p53 (显示 TP53 ELISA试剂盒) and caspase-3 (显示 CASP3 ELISA试剂盒) activation.
Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 (显示 IL10 ELISA试剂盒) production through p38 MAPK activation.
JNK (显示 MAPK8 ELISA试剂盒) 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 (显示 MAPK1/3 ELISA试剂盒), in the neuroretina and retinal arteries.
cytochrome c (显示 CYCS ELISA试剂盒) microinjection induces p38 phosphorylation through caspase-3 (显示 CASP3 ELISA试剂盒) activation, and caspase (显示 CASP3 ELISA试剂盒) 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