Aperçu des produits pour anti-MAPK14 (MAPK14) Anticorps

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

1. p38-mediated phosphorylation at threonine 367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis.

2. High expression of p38MAPK is associated with diabetic cataract.

3. p38 capital EM, Cyrilliccapital A, Cyrilliccapital ER, Cyrilliccapital KA, Cyrillic participates in the pathogenesis of epithelial-to-mesenchymal transition through Wnt pathway.

4. The Cox proportional hazard models revealed that IL12Rb2 and p38MAPK predicted a long OS. To the best of our knowledge, the present study is the first to reveal a close association between IL12Rb2 and p38MAPK, and their possible function in nonsmall cell lung cancer progression

5. Data show that miR-625-3p induces oxaliplatin resistance by abrogating MAP2K6-p38-regulated apoptosis and cell cycle control networks.

6. Immune profiling of human prostate epithelial cells in health and pathology determined by expression of p38/TRAF-6/ERK MAP kinases pathways has been reported.

7. The cytotoxicity induced by EB1 gene knockdown was due to the activation and generation of reactive oxygen species by p38 mitogen-activated protein kinase..this signaling cascade, however not nuclear factor-kappaB-mediated signaling, induced the expression of cyclooxygenase-2, a key effector of apoptotic death.

8. Data, including data using network analysis, suggest that angiotensinogen (AGT), mitogen-activated protein kinase-14 (MAPK14), and prothrombin (F2) in placental villous tissues are core factors in early embryonic development; these studies involved proteomics and bioinformatics analysis of altered protein expression in placental villous tissue from early recurrent miscarriage patients in comparison to control tissues.

9. The role of p38 MAP kinase signaling in metastatic clear cell renal cell carcinoma

10. Rhythmic luciferase activity from clock gene luciferase reporter cells lines was used to test the effect of p38 MAPK inhibition on clock properties as determined using the damped sine fit and Levenberg-Marquardt algorithm.Glioma treatment with p38 MAPK inhibitors may be more effective and less toxic if administered at the appropriate time of the day.

11. Hsp27 and P38MAPK could be used as prognostic factors in Esophageal squamous cell carcinoma.

12. High p38MAPK expression is associated with non-small cell lung cancer metastasis.

13. when the cells were treated with SB203580, an inhibitor of the p38 MAPK pathway, the osteogenic effects of Epo on hPDLSCs and pPDLSCs were attenuated. In conclusion, Epo may upregulate the bone formation ability of hPDLSCs and pPDLSCs via the p38 MAPK pathways

14. p38alpha and ATF2 expression play a crucial role in the malignant phenotypes of ovarian tumor cells and are a markers of poor prognosis in patients with ovarian serous adenocarcinomas.

15. KLF4 overcomes tamoxifen resistance by suppressing MAPK signaling pathway and predicts good prognosis in breast cancer.

16. These results suggest that PYP treatment had a preventive effect on nephrotoxicity, specifically by downregulating the MAPK and NFkappaB signaling pathways and the mRNA levels of inflammatory genes

17. hepatic p38alpha MAPK functions as a negative regulator of liver steatosis in maintaining hepatic bile acid synthesis and fatty acid beta-oxidation by antagonizing the c-Jun N-terminal kinase (JNK).

18. The results reveal a new connection between p38MAPK, MYC and NOTCH signaling, demonstrate two mechanisms of NOTCH3 regulation and provide evidence for NOTCH3 involvement in prostate luminal cell differentiation.

19. Overall, these results suggest that p53 is involved in improving insulin sensitivity of hepatic cells via inhibition of mitogen-activated protein kinases (MAPKs) and NF-kappaB pathways.

20. Data show that the combination of targeting RAD51 and p38 inhibits cell proliferation both in vitro and in vivo, which was further enhanced by targeting of PARP1.

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. Lysosomal p38 MAPK directly phosphorylates LAMP2A at T211 and T213, which causes its membrane accumulation and active conformational change, activating chaperone-mediated autophagy.

2. p38-mediated phosphorylation at threonine 367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis.

3. Results implicate neuronal p38alpha signaling in the synaptic plasticity dysfunction and memory impairment observed in 5XFAD mice, by regulating both amyloid-beta deposition in the brain and the relay of this accumulation to mount an inflammatory response, which leads to the cognitive deficits.

4. These findings uncovered the molecular mechanisms by which p38alpha MAPK regulates osteoclastogenesis and coordinates osteoclastogenesis and osteoblastogenesis.

5. Praja1 promotes skeletal myogenesis through degradation of EZH2 upon p38alpha activation.

6. These results suggested that the thrombinstimulated synthesis of IL6 was limited by HSP90 in osteoblasts, and that the effects of HSP90 were exerted at the point between Rhokinase and p38 MAPK.

7. Overall, the authors showed that CCN1 increased IL-1beta production via p38 MAPK signaling, indicating a role for CCN1 protein in regulating inflammation in psoriasis.

8. we have identified novel interaction between p38 MAPK and Runx2 enhances Runx2 transactivity, thus promoting vascular smooth muscle cells calcification

9. p38alpha MAPK maintains the expression of antioxidant genes in liver of young animals via NF-kappaBeta under basal conditions, whereas its long-term deficiency triggers compensatory up-regulation of antioxidant enzymes through NF-kappaBeta.

10. the present findings suggested that artesunate may exert protective effects against cerebral ischemia/reperfusion injury through the suppression of oxidative and inflammatory processes, via activating Nrf2 and downregulating ROSdependent p38 MAPK in mice.

11. Results show that the p38 MAPK signaling pathway could regulate mitochondria Abeta internalization by manipulating the expression of alpha7nAChR. Pretreatment of alpha7nAChR agonist could attenuate these biochemical changes which are tightly associated with Abeta1-42 induced apoptosis. Suggesting there is an endogenous, previously unrecognized cholinergic mechanism to control mitochondria functions and their apoptotic ...

12. Prdx1 knockout can aggravate the oxidative stress and lung injury by increasing the level of Reactive Oxygen Species (ROS), and also activate P38/JNK signaling pathway.

13. P38 kinase role in the inflammatory pain.CXCL13, upregulated by peripheral inflammation, acts on CXCR5 on dorsal root ganglia neurons and activates p38, which increases Nav1.8 current density and further contributes to the maintenance of inflammatory pain.

14. these findings indicate that BMS309403 reduces fatty acid-induced ER stress-associated inflammation in skeletal muscle by reducing p38 MAPK activation.

15. report insulin-like growth factor-II binding protein 1 (IGF2BP1) as a novel interacting partner of p38 MAPK.

16. These results were supported by the opposite outcomes observed for cells treated with A779 or DX600. Therefore, it was concluded that the ACE2-Ang(17)-Mas axis significantly inhibits pancreatitis by inhibition of the p38 MAPK/NF-kappaB signaling pathway

17. results suggest that c-Jun, p38 MAPK, PIK3CA/Akt, and GSK3 signaling involved in the effect of miR-203 on the proliferation of hepatocellular carcinoma cells.

18. The Macrophage Activation Induced by Bacillus thuringiensis Cry1Ac Protoxin Involves ERK1/2 and p38 Pathways and the Interaction with Cell-Surface-HSP70

19. MAPK in, and found that p38alpha deficiency causes Th1 cells to hyperproliferate via the Mnk1/eIF4E pathway

20. B7-H1 suppresses p38 MAPK activation by sequestering DNA-PKcs in order to preserve T cell survival

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.