• Reactive oxygen species-mediated p38 MAPK regulates carbon nanotube -induced fibrogenic and angiogenic responses. (cdc.gov)
  • SWCNTs induce fibrogenesis through reactive oxygen species-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK). (cdc.gov)
  • Activation of p38 MAPK by SWCNTs led to the induction of transforming growth factor (TGF)-b1 as well as vascular endothelial growth factor (VEGF). (cdc.gov)
  • In malignant biliary tract epithelia, IL-6 activates the p38 MAPK pathway, which mediates a dominant survival signaling pathway. (elsevierpure.com)
  • After IL-6 stimulation, p38 MAPK activation preceded phosphorylation of SGK at Ser 78 . (elsevierpure.com)
  • Pretreatment with the pharmacological inhibitors of p38 MAPK SB-203580 or SB-202190 blocked IL-6-induced SGK phosphorylation at Ser 78 and SGK activation. (elsevierpure.com)
  • Overexpression of p38α increased constitutive SGK phosphorylation at Ser 78 , whereas dominant negative p38α MAPK blocked IL-6-induced SGK phosphorylation and nuclear translocation. (elsevierpure.com)
  • Interestingly, in addition to stimulating SGK phosphorylation, both IL-6 stimulation and p38α MAPK overexpression increased SGK mRNA and protein expression. (elsevierpure.com)
  • An increase in p38 MAPK and SGK occurred following enforced expression of IL-6 in vivo. (elsevierpure.com)
  • Taken together, these data identify SGK as both a downstream kinase substrate as well as a transcriptionally regulated gene target of p38 MAPK in response to IL-6 and support a role of SGK during survival signaling by IL-6 in human cancers, such as cholangiocarcinoma. (elsevierpure.com)
  • The present study explored the effect of NAC on LPS‑induced apoptosis of HUVECs and determined the participation of the p38 mitogen‑activated protein kinase (MAPK) pathway in the process of apoptosis. (spandidos-publications.com)
  • Nigericin also induced both an increase in phosphorylated p38 MAPK and proteasomal degradation of ß-catenin. (bvsalud.org)
  • In the present study, we investigated whether contractions of isolated muscles induced phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and p38 MAPK in a fibre-type dependent manner. (elsevierpure.com)
  • Significant increase in phosphorylation of p38 MAPK was observed in the fast-twitch muscles only. (elsevierpure.com)
  • The total amount of ERK1/2 and p38 MAPK proteins was higher in the slow-twitch soleus muscle. (elsevierpure.com)
  • The opioid receptor activation regulates a variety of intracellular signaling, including the mitogen-activated protein kinase (MAPK) pathway. (iasp-pain.org)
  • In addition, astragalus saponins also suppressed the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and inhibited nuclear factor kappaB (NF-?B) activation and the associated I?B? (research.news)
  • Overall, astragalus saponins can inhibit LPS-induced inflammatory responses by regulating p38 MAPK signaling and suppressing NO and cytokine release. (research.news)
  • Stimulation of heterophils with each specific TLR agonist led to a differential increase in the phosphorylation of both p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 (ERK 1/2) activation, but not the phosphorylation of c-Jun NH2-terminal kinase (JNK). (ox.ac.uk)
  • Non-canonical or alternative type I IFN signaling can activate additional pathways such as Crk-like protein (CrkL), the phosphatidyl-inositol 3-kinase (PI3K) pathway, and the mitogen-activated protein kinase (MAPK) pathway [ 15 ]. (scientificarchives.com)
  • Changes in ST mitogen-activated protein kinase (MAPK) activation were assessed by immunoblotting and mRNA expression levels of selected cytokine and chemokines in primary ST bound by iRBC were determined using real-time, reverse transcription PCR. (biomedcentral.com)
  • Inhibitors of p38 and p44/42 mitogen-activated protein kinase (MAPK) activation inhibited CRP expression, implicating the involvement of both pathways in cytokine-induced CRP expression. (lacienciadelvino.com)
  • Los inhibidores de la proteína p38 y p44/42 mitógeno-quinasa activada (MAPK) inhibe la activación de la expresión de CRP, que implican la participación de ambas vías en la expresión inducida por citocinas CRP. (lacienciadelvino.com)
  • Estos datos revelaron una función previamente desconocida de la vía de señalización MAPK p44/42 en la expresión de proteína C reactiva. (lacienciadelvino.com)
  • We previously showed that prostaglandin E1 (PGE1) induces the synthesis of IL-6 by activating p44/p42 mitogen-activated protein kinase (MAPK), stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and p38 MAPK in osteoblast-like MC3T3-E1 cells. (iasp-pain.org)
  • In the present study, we investigated whether heat shock protein 70 (HSP70), a molecular chaperone that coordinates protein folding and homeostasis, affects PGE1-stimulated IL-6 synthesis in MC3T3-E1 cells through the MAPK activation. (iasp-pain.org)
  • The phosphorylation of p38 MAPK was evaluated by Western blotting. (iasp-pain.org)
  • On the other hand, SB203580, a p38 MAPK inhibitor, suppressed PGE1-stimulated IL-6 release. (iasp-pain.org)
  • YM-08 stimulated the PGE1-induced phosphorylation of p38 MAPK. (iasp-pain.org)
  • Our results suggest that HSP70 inhibitors upregulate the PGE1-stimulated IL-6 synthesis through p38 MAPK in osteoblasts and therefore affect bone remodeling. (iasp-pain.org)
  • Protein kinase D1 (PKD1), together with PKD2 and PKD3, constitute a family classified within the calcium/calmodulin-dependent protein kinase superfamily 7 . (nature.com)
  • With HG, phosphorylation of filamin likely contributed to the cortical actin disassembly, whereas Ca 2+ /calmodulin-dependent protein kinase II and p38 mitogen-activated protein kinase/heat shock protein 25 phosphorylation mediated stress actin formation. (ewha.ac.kr)
  • For p38 beta, also known as p38-2, stress-activated protein kinase 2B (SAPK2B), and MAPK11, this dual phosphorylation occurs at Thr180/Tyr182. (rndsystems.com)
  • 2007. p38 mitogen-activates protein kinase controls NF-kB transcriptional activation and tumor necrosis factor alpha production through RelA phosphorylation mediated by mitogen-and stress activated protein kinase 1 in response to Borrelia burgdorferi antigens. (charlotte.edu)
  • On the other hand, an increase in Ca 2+ induces eNOS translocation from the cell membrane to the cytosol or Golgi complex ( 8 ), where it is phosphorylated and fully activated by protein kinases that reside in caveolae, such as p38 mitogen-activated protein kinase, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), cAMP-dependent protein kinase A, and 5′ AMP-activated protein kinase ( 7 ). (diabetesjournals.org)
  • The activities of mitogen-activated protein kinase kinase (MAPKK) 4 and phosphatidylinositol-3 kinase (PI-3K) were inhibited markedly by delphinidin. (oregonstate.edu)
  • Compared with the contralateral non-stimulated muscle, contractions increased ERK1/2 phosphorylation to the same extent in fast- and slow-twitch muscles. (elsevierpure.com)
  • Using primary cultures of sensory neurons, it was demonstrated that crotalphine increases the level of activated ERK1/2 and JNK-MAPKs and this increase is dependent on the activation of protein kinase Cζ (PKCζ). (iasp-pain.org)
  • Here, we biochemically demonstrated that the systemic crotalphine activates ERK1/2 and JNK and decreases the phosphorylation of p38 in the lumbar spinal cord. (iasp-pain.org)
  • The in vivo pharmacological inhibition of spinal ERK1/2 and JNK, but not of p38, blocks the antinociceptive effect of crotalphine. (iasp-pain.org)
  • siRNA-mediated knockdown (KD) of TRAF2 in INS-1E cells reduced IL-1β-induced phosphorylation of JNK1/2, but not of p38 or ERK1/2 mitogen-activated protein kinases. (ku.dk)
  • In the human monocytic MonoMac 6 cell line, 4-HNE caused selective inhibition of the activity of the mitogen-activated protein kinases p38 and ERK1/ERK2, but not JNK. (monocyte.eu)
  • However, in monocytes, the activities of all three kinases were inhibited, suggesting that the effects of 4-HNE were exerted at points upstream of ERK1/ERK2 and JNK as the levels of the phosphorylated kinases were reduced. (monocyte.eu)
  • In view of the roles of p38, ERK1/ERK2, JNK, and nuclear factor-kappaB in inflammation, the data suggest that 4-HNE, at nontoxic concentrations, has anti-inflammatory properties, most likely through an effect on these signaling molecules, and could lead to the development of novel treatments for inflammatory diseases. (monocyte.eu)
  • Compared with BBR, dhBBR and Di-MeBBR significantly reduced EMMPRIN expression, which was associated with a greater inhibition of p-p38, p-JNK, nuclear NFκB p65 and phospho-p65 induced by oxLDL in macrophages. (biomedcentral.com)
  • Here, we show that, in addition to its kinase activity, TAK1 has intrinsic ATPase activity, that (5Z)-7-Oxozeaenol irreversibly inhibits TAK1, and that sensitivity to (5Z)-7-Oxozeaenol inhibition in hematological cancer cell lines is NRAS mutation status and TAK1 pathway dependent. (rcsb.org)
  • Detailed biochemical characterization revealed that (5Z)-7-Oxozeaenol inhibited both the kinase and the ATPase activity of TAK1 following a bi-phase kinetics, consistent with the irreversible inhibition mechanism. (rcsb.org)
  • In DoHH2 cells, (5Z)-7-Oxozeaenol potently inhibited the p38 phosphorylation driven by TAK1, and the inhibition lasted over 6 h after withdrawal of (5Z)-7-Oxozeaenol. (rcsb.org)
  • Delphinidin suppresses ultraviolet B-induced cyclooxygenases-2 expression through inhibition of MAPKK4 and PI-3 kinase. (oregonstate.edu)
  • This study is to investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in tert -butyl hydroperoxide ( t BHP)-induced apoptosis of human trabecular meshwork (iHTM) cells. (molvis.org)
  • Activation of p38MAPK plays an important role in t BHP-induced apoptosis of iHTM cells. (molvis.org)
  • In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
  • The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • The expression of caspase‑3, Bax, Bcl‑2, phosphorylated (p)‑p38MAPK/total (t‑)p38MAPK and p‑endothelial e nitric oxide synthase (eNOS)/t‑eNOS proteins were determined by western blotting. (spandidos-publications.com)
  • Results: TSA activated p38 mitogen-activated protein kinase (p38MAPK), leading to p53 phosphorylation and activation. (tmu.edu.tw)
  • Conclusions: TSA may cause C6 cell apoptosis through activating p38MAPK-p53 cascade resulting in Bax expression and survivin suppression. (tmu.edu.tw)
  • Strategies for managing steroid resistance include alternative anti-inflammatory drugs, but a novel approach is to reverse steroid resistance by increasing HDAC2 expression, which can be achieved with theophylline and phosphoinositide 3-kinase δ inhibitors. (nih.gov)
  • Numerous stimuli activate PKD through well-established pathways. (nature.com)
  • Activation of mitogen-activated protein (MAP) kinases has been implicated in the signal transduction pathways linking exercise to adaptive changes of muscle protein expression. (elsevierpure.com)
  • In conclusion, MAP kinase signalling pathways are differentially activated and expressed in slow- and fast-twitch muscles. (elsevierpure.com)
  • Since glucocorticoids are essential for life, other cellular signaling pathways strongly regulate GR actions in many different ways, such as physical interaction via their effector transcription factors and epigenetic modifications including phosphorylation and acetylation. (brainimmune.com)
  • Type I IFN-induced activation of JAK/STAT pathways is a complex process and not well understood. (scientificarchives.com)
  • Transforming growth factor-β activated kinase-1 (TAK1) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family that regulates several signaling pathways including NF-κB signal transduction and p38 activation. (rcsb.org)
  • Investigation of signaling pathways showed that the cytokines induced the phosphorylation of p38 and p44/42 MAP kinases. (lacienciadelvino.com)
  • Since oxidative stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity. (nature.com)
  • Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
  • EPO activates the neuronal EPO receptor and, subsequently, JAK-2 and thereby PI3K. (jneurosci.org)
  • Mutant SOD1 activated neuronal p38 in mouse spinal cord, neuroblastoma cells and squid axoplasm. (mblwhoilibrary.org)
  • The human trabecular meshwork cells were treated with t BHP for 1 or 2 h with or without pretreatment of SB203580, an inhibitor of MAP kinase homologs. (molvis.org)
  • In addition, survivin, a member of inhibitor of apoptotic protein, was significantly decreased in TSA-treated C6 cells. (tmu.edu.tw)
  • Cultured neurons express EpoR, and the Janus kinase-2 (JAK-2) inhibitor AG490 abolished EPO-induced tolerance against OGD. (jneurosci.org)
  • Furthermore, EPO-induced neuroprotection as well as phosphorylation of the proapoptotic Bcl family member Bad was reduced by the phosphoinositide-3 kinase (PI3K) inhibitor LY294002. (jneurosci.org)
  • Of interest, the administration of a PKCζ pseudosubstrate (PKCζ inhibitor) prevents crotalphine-induced ERK activation in the spinal cord, followed by the abolishment of crotalphine-induced analgesia. (iasp-pain.org)
  • Cell surface EMMPRIN expression was measured by flow cytometry and Western blotting, and phospho-(p)-p38, p-JNK, nuclear NFκB p65, and phospho-p65 were measured by Western blotting. (biomedcentral.com)
  • 4-HNE also inhibited nuclear factor-kappaB activation in monocytes. (monocyte.eu)
  • Activator protein-1 and nuclear factor-kappaB, crucial transcription factors involved in COX-2 expression, were activated by UVB and delphinidin abolished this activation. (oregonstate.edu)
  • This article reviews the anti-inflammatory relative and anti-infectious effects of Evodia rutaecarpa and its major bioactive components and the involvement of the nitric oxide synthases, cyclooxygenase, NADPH oxidase, nuclear factor kappa B, hypoxia-inducible factor 1 alpha, reactive oxygen species, prostaglandins, tumor necrosis factor, LIGHT, amyloid protein and orexigenic neuropeptides. (biomedcentral.com)
  • Type I IFNs initiate their biological effects by binding to their transmembrane interferon receptors and initiating the phosphorylation and activation of tyrosine kinases TYK2 and JAK1, which promote phosphorylation and activation of STAT molecules. (scientificarchives.com)
  • Studies have shown that all type I IFNs exclusively bind to and signal through ubiquitously expressed heterodimeric transmembrane (TM) receptors composed of two subunits-IFNAR1 and IFNAR2 [ 3 ], which are constitutively associated with tyrosine kinases TYK2 and JAK1/STAT2 (signal transducer and activator of transcription 2), respectively, under normal physiological conditions [ 4 , 5 ]. (scientificarchives.com)
  • Upon binding of type I IFNs to IFNAR1 and IFNAR2, the proximal receptor complex is assembled and the tyrosine kinases TYK2 and JAK1 are activated by reciprocal transphosphorylation. (scientificarchives.com)
  • SYK, along with ZAP70, is a member of the Syk family of tyrosine kinases. (syksignaling.com)
  • HDAC2 appears to mediate the action of steroids to switch off activated inflammatory genes, but in patients with COPD, patients with severe asthma, and smokers with asthma, HDAC2 activity and expression are reduced by oxidative stress through activation of phosphoinositide 3-kinase δ. (nih.gov)
  • The p38 mitogen-activated protein kinases (p38 MAP kinases) are a family of four related Ser/Thr kinases responsive to pro-inflammatory cytokines and environmental stresses, including ionizing radiation, oxidative stress, and osmotic shock. (rndsystems.com)
  • Oxidative stress is an important activator of PKD1 in cellular models, but its capacity to activate this kinase in vivo is largely unknown. (nature.com)
  • Of note, DAPK can activate PKD in HeLa cells under oxidative stress conditions 11 , thus suggesting that PKD activation may contribute to cellular death. (nature.com)
  • The N-terminal tyrosine of dynorphin A is necessary to activate opioid receptors such as KOR, but is unnecessary in binding to bradykinin receptors. (wikipedia.org)
  • NO production in response to various factors, such as increased shear stress, is mediated by endothelial nitric oxide synthase (eNOS), which is constitutively expressed in endothelial cells (ECs) and is tightly controlled by various membrane-bound receptors and regulatory proteins under physiological conditions ( 3 ). (diabetesjournals.org)
  • Odorant receptors (ORs) are G protein-coupled receptors (GPCRs) that are essential for detecting and distinguishing among odorants. (bmbreports.org)
  • Receptors in the posterior pharynx are then activated to initiate the involuntary phase of deglutition, which involves carefully sequenced contraction of numerous head and neck muscles. (nature.com)
  • This peptide induces a potent and long-lasting antinociceptive effect that is mediated by the activation of peripheral opioid receptors. (iasp-pain.org)
  • Tumor necrosis factor (TNF) receptor-associated factor (TRAF) proteins are adaptors that transduce signaling from a variety of membrane receptors including cytokine receptors. (ku.dk)
  • Following iRBC/ST interaction, ST C-Jun N-terminal kinase 1 (JNK1) was activated and modest increases in the mRNA expression of TGF-β and IL-8/CXCL8 were observed. (biomedcentral.com)
  • Astragalus also consistently reduced the gene and protein overexpression of inducible NO synthase (iNOS), as well as the production of tumor necrosis factor-alpha induced by LPS. (research.news)
  • The protein level of phospho-p38 was measured using western blot analysis. (molvis.org)
  • Detection of Human, Mouse, and Rat p38 beta by Western Blot. (rndsystems.com)
  • Western blot shows Recombinant Human p38 beta, Recombinant Human p38? (rndsystems.com)
  • Type I IFN-activated JAK1/TYK2 also induces rapid phosphorylation and activation of insulin receptor substrate 1 (IRS1) and 2 (IRS2), which subsequently bind to the catalytic p85 subunit of PI3K, which is required for the activation of the regulatory p110 subunit of PI3K [ 20 ]. (scientificarchives.com)
  • Zellzerst Tion by lowering eIF2 and PERK-dependent Ngigen protein c-flip-plane, w While the overexpression of c-flips Zelllebensf Get up ability. (syksignaling.com)
  • showed that the expression of phosphorylation-insensitive eIF2 S51A sorafenib and vorinostat L research abolished by blocking c-flips induced levels and the overexpression of c-flips lethality t. overexpression of c-flip suppression zellt important function of multinuclear platinum WZ8040 chemotherapeutic BBR3610. (syksignaling.com)
  • General significance: TSA-induced p53 activation may occur through p53 modification by phosphorylation or by acetylation via IKK inactivation. (tmu.edu.tw)
  • In many cases this activation is transient, but the mechanisms stopping sustained stimulation remain unexplored 7 . (nature.com)
  • Although activated TYK2 and JAK1 phosphorylate and activate STAT2, which is a critical early step for STAT1 activation by type I IFN in canonical signaling [ 6 ], the mechanism of STAT2-dependent STAT1 activation after stimulation of type I IFN is poorly understood. (scientificarchives.com)
  • It is now recognized that a major mechanism involved in eNOS activation is phosphorylation of eNOS at the Ser 1177 residue ( 1 , 2 ). (diabetesjournals.org)
  • Unexpectedly, we find that excitotoxicity provokes an early inactivation of PKD1 through a dephosphorylation-dependent mechanism mediated by protein phosphatase-1 (PP1) and dual specificity phosphatase-1 (DUSP1). (nature.com)
  • The antiadipogenic mechanism of endostatin lies in its interaction with Sam68 RNA-binding protein in the nuclei of preadipocytes. (diabetesjournals.org)
  • The central mechanism involves patterned activation of the preganglionic neurons in the dorsal motor nucleus of the vagus that project onto inhibitory and excitatory neurons in the esophageal myenteric plexus. (nature.com)
  • Here we show that polyQ-Htt inhibits FAT through a mechanism involving activation of axonal JNK. (mblwhoilibrary.org)
  • Experiments in isolated squid axoplasm reveal that FALS-related SOD1 mutant polypeptides inhibit FAT through a mechanism involving a p38 mitogen activated protein kinase pathway. (mblwhoilibrary.org)
  • In addition to subcellular location and protein-protein interactions, several phosphorylation and dephosphorylation sites also modulate eNOS activity ( 9 ). (diabetesjournals.org)
  • TRAF2 KD did not modulate NFκB activation by cytokines, but reduced cytokine-induced inducible nitric oxide synthase (iNOS) promotor activity and expression. (ku.dk)
  • BACKGROUND: Elevation of C-reactive protein (CRP) levels in blood was recognized as one of the cardiac disease risk factors. (lacienciadelvino.com)
  • Accordingly, increased activation of JNK was observed in vivo in cellular and animal HD models. (mblwhoilibrary.org)
  • ATP release, purinergic receptor activation, cortical actin disassembly, and stress actin formation were essential for this HG-induced heparanase secretion. (ewha.ac.kr)
  • Adenosine is metabolized by adenosine deaminase and adenosine kinase. (dissertations.se)
  • We provide evidence for the following signaling cascade: HIF-1 is activated rapidly by hypoxia in astrocytes. (jneurosci.org)
  • P53, a proapoptotic transcription factor, in turn transactivated the expression of a proapoptotic protein, Bax. (tmu.edu.tw)
  • By two-dimensional gel electrophoretic analysis of synaptosomal fractions from transgenic mouse brains we detected additional isoforms of septin 6, a downstream target of Cdc42 effector proteins. (proteasomesignaling.com)
  • Aortic atherosclerotic lesion size, plaque matrix proteins, and EMMPRIN and other inflammatory factors were measured using Oil Red O Staining, Masson's trichromestaining and immunohistochemical staining and real-time PCR. (biomedcentral.com)
  • Atherosclerosis starts with dysfunctional changes in the endothelium induced by disturbed shear stress which can lead to endothelial and platelet activation, adhesion of monocytes on the activated endothelium, and differentiation into proinflammatory macrophages, which increase the uptake of oxidized LDL (oxLDL) and turn into foam cells, exacerbating the inflammatory signalling. (hindawi.com)
  • Sepsis is a systemic inflammatory response caused by a harmful host immune reaction that is activated in response to microbial infections. (scientificarchives.com)
  • In ECs, Cav-1 anchors eNOS in plasma membrane caveolae, which limits its translocation and phosphorylated activation and thereby reduces its capacity to generate NO ( 7 ) ( Fig. 1 ). (diabetesjournals.org)
  • Characteristics of motor neurons affected in FALS include abnormal kinase activation, aberrant neurofilament phosphorylation, and fast axonal transport (FAT) deficits, but functional relationships among these pathogenic events were unclear. (mblwhoilibrary.org)
  • Cdc42 effector proteins were also co-immunoprecipitated with alpha-synuclein from brainstem lysates and were colocalized with alpha-synuclein aggregates in brain sections by double immunostaining. (proteasomesignaling.com)
  • 2006. Control of Borrelia burgdorferi -specific CD4 + T cell effector function by interleukin-12- and T-cell receptor-induced p38 mitogen-activated protein kinase activity. (charlotte.edu)
  • Minocycline is a semi-synthetic second-generation tetracycline known to improve cognition in amyloid precursor protein transgenic mice. (proteasomesignaling.com)
  • Caveolin-1 (Cav-1), an anchoring protein in the plasma membrane caveolae in ECs and vascular smooth muscle cells (VSMCs), attenuates endothelial NO production by occupying the calcium/calmodulin (Ca 2+ /CaM) binding site of eNOS ( 4 ) ( Fig. 1 ). (diabetesjournals.org)
  • KD of TRAF2 or STAT3 reduced cytokine-induced caspase 3/7 activation, but, intriguingly, potentiated cytokine-mediated loss of plasma membrane integrity and augmented the number of propidium iodide-positive cells. (ku.dk)
  • This might be due to modification of the GR by means of phosphorylation as a result of activation of several kinases (p38 mitogen-activated protein kinase α, p38 mitogen-activated protein kinase γ, and c-Jun N-terminal kinase 1), which in turn might be due to reduced activity and expression of phosphatases, such as mitogen-activated protein kinase phosphatase 1 and protein phosphatase A2. (nih.gov)
  • Lipopolysaccharide (LPS) can regulate the expression of apoptotic factors, including caspase‑3, Bcl‑2 and Bcl‑2‑associated X protein (Bax). (spandidos-publications.com)
  • In contrast, p38 phosphorylation was not inhibited, suggesting that 4-HNE affects kinase activity. (monocyte.eu)
  • The endothelial secreted heparanase in response to HG demonstrated endoglucuronidase activity, cleaved heparan sulfate, and released attached proteins like lipoprotein lipase and basic fibroblast growth factor. (ewha.ac.kr)
  • PKCζ-Mitogen-Activated Protein Kinase Signaling Mediates Crotalphine-Induced Antinociception. (iasp-pain.org)
  • Cardiovascular (CV) risk factors such as hypercholesterolemia, hyperglycaemia, obesity, hypertension, smoking, and aging promote vascular inflammation and endothelial activation [ 7 - 9 ]. (hindawi.com)
  • Type I IFN activated STAT1 and STAT2 also form other heterodimers, including STAT1-STAT3, STAT1-STAT4, STAT1-STAT5, and STAT2-STAT3 in specific cell types such as endothelial cells or cells of lymphoid origin [ 3 , 12 - 14 ]. (scientificarchives.com)
  • Dynorphins exert their effects primarily through the κ-opioid receptor (KOR), a G-protein-coupled receptor. (wikipedia.org)
  • Contraction is a multifactorial stimulus with short-term metabolic effects and long-term responses due to changes in protein synthesis. (dissertations.se)
  • Apart from endothelium dependence, alpha 1-adrenoceptor blockade, K + channel activation and Ca 2+ channel blockade were also involved in the vasorelaxant effect of DeHE [ 7 ]. (biomedcentral.com)
  • Coupled with influx of extracellular calcium, Rut produced the endothelium-dependent vasorelaxant effect by activation of endothelium NOS and release of NO without pertussis toxin-sensitive Gi protein and other G proteins or phospholipase C activation being involved [ 8 ]. (biomedcentral.com)
  • 2007. C-Jun N-terminal kinase is required for TLR 1 gene transcription in macrophages. (charlotte.edu)
  • Type I IFN- activated STAT1 can also form a homodimer known as IFNγ-Activated Factor (GAF), which migrates into the nucleus, and binds to IFNγ-Activated Sequences (GAS), to induce proinflammatory genes [ 10 , 11 ]. (scientificarchives.com)
  • Long-acting β2-agonists can also increase steroid responsiveness by reversing GRα phosphorylation. (nih.gov)