Aperçu des produits pour anti-MAPK14 (MAPK14) Anticorps

Human Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. Deletion of p38alphaMAPK in microglia only, was sufficient to attenuate inflammatory responses following traumatic brain injury.

2. 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

3. Aryl hydrocarbon receptor activation does not mediate skatole-induced ERK, p38 and JNK activation in intestinal epithelial cells.

4. 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.

5. 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

6. 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.

7. Ablation of DeltaNp63 alpha leads to cell cycle arrest and growth retardation, due to, in part, upregulation of p38 MAPK phosphorylation and activation.

8. p38alpha destabilizes p63 to limit epidermal stem cell frequency and tumorigenic potential

9. 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)

10. 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.

11. 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.

12. Ngb promotes axon regeneration via oxygen-Ngb-p38-GAP43 signaling during ischemia/reperfusion.

13. It is a serine/threonine-specific protein kinase that transduces intracellular signals in critical cellular phenomena.

14. 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.

15. Cadmium promotes colon cancer cell migration through ROS-dependent activation of p38 MAPK.

16. 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.

17. 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.

18. 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.

19. 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.

20. These observations indicate that p38alpha probably blocks brown adipose tissue thermogenesis through p38delta inhibition.

Zebrafish Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. P38 and JNK have opposing effects on persistence of in vivo leukocyte migration in zebrafish.

2. Adult zebrafish cardiomyocytes express active p38alpha MAPK, which is switched off upon entry into mitosis.

3. Dkk3r regulates p38a phosphorylation to maintain Smad4 stability, in turn enabling the Smad2.Smad3a.Smad4 complex to form and activate the myf5 promoter.

Cow (Bovine) Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. 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

2. 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.

3. MAPK14 signalling pathway is largely involved in heat-induced sperm damage.

4. p38 MAPK is an early redox sensor in the laminar shear stress with hydrogen peroxide being a signaling mediator.

5. Blockade of p38 enhances chondrocyte phenotype in monolayer culture and may promote more efficient cartilage tissue regeneration for cell-based therapies.

6. 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.

7. These data suggest that the p38 and JNK signaling pathways play pivotal roles in PRRSV replication and may regulate immune responses during virus infection.

8. findings support the hypothesis that ischemic factor stimulation of the blood-brain barrier Na-K-Cl cotransporter involves activation of p38 and JNK MAPKs

9. 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.

10. p38 MAPK (MAPK14) is redox-regulated in reactive oxygen species-dependent endothelial barrier dysfunction.

11. involvement of p38 MAP kinase activities and caldesmon phosphorylation in the MLCK-independent regulation of thrombin-induced endothelial cell permeability.

12. involvement of p38 MAP kinase in the hyaluronan oligosaccharide induction of MMP-13

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.

14. Replacement of distention with pharmacological relaxation reduced the increase in p38 expression, but not extracellular signal-regulated kinases.

15. 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

16. 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

17. Thrombospondin 1, fibronectin, and vitronectin are differentially dependent upon RAS, ERK1/2, and p38 for induction of vascular smooth muscle cell chemotaxis.

Fruit Fly (Drosophila melanogaster) Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. These results illustrate a novel pro-tumourigenic crosstalk between the p38 MAPK pathway and JAK signalling in a Drosophila model of Myeloproliferative neoplasms.

2. ROS/JNK/p38/Upd 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.

3. 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.

4. data suggest that p38Kb may affect circadian locomotor rhythms through the regulation of multiple downstream pathways

5. Data show that the genetic interaction between p38b MAPK and Rack1 controls muscle aggregate formation, locomotor function, and longevity.

6. The interaction of any of several Drosophila Delta class glutathione transferases and p38b mitogen-activated protein kinase can affect the substrate specificity of either enzyme, which suggests induced conformational changes affecting catalysis.

7. 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

8. Loss of p38 MAPK causes early lethality and precipitates age-related motor dysfunction and stress sensitivity.

9. The p38 pathway-mediated stress response contribute to Drosophila host defense against microbial infection.

10. p38b MAPK plays a crucial role in the balance between intestinal stem cell proliferation and proper differentiation in the adult Drosophila midgut.

11. the D-p38b gene is regulated by the DREF pathway and DREF is involved in the regulation of proliferation and differentiation of Drosophila ISCs and progenitors

Mouse (Murine) Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. findings indicate that cell-permeable p38 protein may be useful in preventing the degeneration of higher brain function occurring through hippocampal neuronal cell death.

2. 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

3. 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.

4. 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.

5. data suggest that Caspase-3 inhibits chemical-induced hepatocarcinogenesis by suppressing p38 activation and hepatocyte death.

6. alpha-synucleinA53T overexpression caused p38 MAPK activation, then p38 MAPK directly phosphorylated Parkin at serine 131 to disrupt the Parkin's protective function.

7. 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.

8. neuronal p38alpha negatively regulates JNK activity that is required for specific modulation of anxiety-related behaviour.

9. 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.

10. 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.

11. 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.

12. cisplatin activates TAK1, which phosphorylates p38 and ERK, leading to excessive autophagy of tubular epithelial cells that exacerbates kidney damage.

13. 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.

14. this study shows that p38alpha has an important role in antigen cross-presentation by dendritic cells

15. 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

16. 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.

17. Ngb promotes axon regeneration via oxygen-Ngb-p38-GAP43 signaling during ischemia/reperfusion.

18. These results indicate that natriuretic peptide exerts a renoprotective effect via inhibiting phosphorylation of p38 MAPK in podocytes.

19. High p38MAPK expression is associated with abdominal aortic aneurysm.

20. These observations indicate that p38alpha probably blocks brown adipose tissue thermogenesis through p38delta inhibition.

Xenopus laevis Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. cytochrome c microinjection induces p38 phosphorylation through caspase-3 activation, and caspase inhibition reduces p38 activation induced by osmostress, indicating that a positive feedback loop is engaged by hyperosmotic shock

Horse (Equine) Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. p38 mitogen-activated protein kinase is crucial for bovine papillomavirus type-1 transformation of equine fibroblasts.

2. p38 Mitogen-activated protein kinase (MAPK) is essential for drug-induced COX-2 expression in leukocytes, suggesting that p38 MAPK is a potential target for anti-inflammatory therapy.

3. 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.

4. Cultured equine digital vein endothelial cells were exposed to lipopolysaccharide and phosphorylation of p38 MAPK was assessed by Western blotting using phospho-specific antibodies.

Pig (Porcine) Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. The results of the current study indicate that dioscin may protect against coronary heart disease by regulating oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways.

2. Porcine reproductive and respiratory syndrome virus strain CH-1a could significantly up-regulate IL-10 production through p38 MAPK activation.

3. JNK plays an active role in fragmentation of pig oocytes and p38 MAPK is not involved in this process.[p38MAPK]

4. Retinal ischemia-reperfusion alters expression of mitogen-activated protein kinases, particularly ERK1/2, in the neuroretina and retinal arteries.

Rabbit Mitogen-Activated Protein Kinase 14 (MAPK14) interaction partners

1. These findings suggest that the TQ-induced production of ROS causes dedifferentiation through the ERK pathway and inflammation through the PI3K and p38 pathways in rabbit articular chondrocytes.

2. 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, p53 and caspase-3 activation.