Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _3 value "As previously reported, expression of IL-6R mRNA in rat Sertoli cells was stimulated not only by IL-1-beta and IL-6 but also by FSH." provenance.
- _5 value "Il6 activates STAT1 and STAT5 in addition to STAT3" provenance.
- _5 value "Il6 activates STAT1 and STAT5 in addition to STAT3" provenance.
- _5 value "JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to Il6, CNTF, LIF, and OSM" provenance.
- _6 value "JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to Il6, CNTF, LIF, and OSM" provenance.
- _6 value "JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to Il6, CNTF, LIF, and OSM" provenance.
- _6 value "JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to Il6, CNTF, LIF, and OSM" provenance.
- _8 value "PIAS proteins constitute a family (PIAS-1, PIAS-3, PIAS-Xalpha, PIAS-Xbeta, and PIAS-Y) of constitutively expressed negative regulators of STATs Pias1 associates only with activated STAT1 dimers and inhibits their DNA-binding activity Pias3 associates specifically with activated STAT3 but not with STAT1, resulting in the blocking of all STAT3-mediated gene transcriptions Pias3 is especially well known as an inhibitor of Il6 signaling in M1 cell lines" provenance.
- _5 value "Socs1 a negative regulatory molecule of Il6 signaling on the basis of its binding to JAK Socs1 directly interacts with JAK1 and JAK2 and thus inhibits their catalytic activity" provenance.
- _5 value "Socs1 a negative regulatory molecule of Il6 signaling on the basis of its binding to JAK Socs1 directly interacts with JAK1 and JAK2 and thus inhibits their catalytic activity" provenance.
- _5 value "Socs1 inhibits activation of STAT6 by Il4 stimulation" provenance.
- _7 value "Socs1 inhibits activation of STAT6 by Il4 stimulation" provenance.
- _8 value "binding of Il6 to Il6R induces homodimerization ofgp130, activating JAK associated with gp130 at Box1.......Our group and others found that JAK1, JAK2, and Tky-2 are activated and are tyrosine-phosphorylated in response to IL-6, CNTF, LIF, and OSM [14]" provenance.
- _4 value "in Il6 signal cascade, the SHP2 interaction site of gp130 has also been shown to be a Socs3 contact site so that Socs3 may compete for the SHP2-gp130 interaction site" provenance.
- _5 value "nonreceptor tyrosine kinases, such as Btk, Tec, Fes, and Hck are activated through the Il6R receptor" provenance.
- _5 value "this is followed by the tyrosine phosphorylation of the distal part of gp130 and recruitment of STAT3 STAT3 is then tyrosine-phosphorylated by JAK" provenance.
- _5 value "tyrosine phosphorylation of SHP2, a phosphotyrosine phosphatase, and that of STAT3 depend on the second tyrosine residue Y2 from the membrane in gp130" provenance.
- _4 value "ATF6 is an endoplasmic reticulum (ER) stress-regulated transmembrane transcription factor that activates the transcription of ER molecular chaperones. Upon ER stress, ATF6 translocates from the ER to the Golgi where it is processed to its active form. We have found that the ER chaperone BiP/GRP78 binds ATF6 and dissociates in response to ER stress. Loss of BiP binding correlates with the translocation of ATF6 to the Golgi, which was slowed in cells overexpressing BiP. Two Golgi localization signals (GLSs) were identified in ATF6. Removal of BiP binding sites from ATF6, while retaining a GLS, resulted in its constitutive translocation to the Golgi. These results suggest that BiP retains ATF6 in the ER by inhibiting its GLSs and that dissociation of BiP during ER stress allows ATF6 to be transported to the Golgi." provenance.
- _4 value "ATF6 is an endoplasmic reticulum (ER) stress-regulated transmembrane transcription factor that activates the transcription of ER molecular chaperones. Upon ER stress, ATF6 translocates from the ER to the Golgi where it is processed to its active form. We have found that the ER chaperone BiP/GRP78 binds ATF6 and dissociates in response to ER stress. Loss of BiP binding correlates with the translocation of ATF6 to the Golgi, which was slowed in cells overexpressing BiP. Two Golgi localization signals (GLSs) were identified in ATF6. Removal of BiP binding sites from ATF6, while retaining a GLS, resulted in its constitutive translocation to the Golgi. These results suggest that BiP retains ATF6 in the ER by inhibiting its GLSs and that dissociation of BiP during ER stress allows ATF6 to be transported to the Golgi." provenance.
- _5 value "We have found that the ER chaperone BiP/GRP78 binds ATF6 and dissociates in response to ER stress. Loss of BiP binding correlates with the translocation of ATF6 to the Golgi, which was slowed in cells overexpressing BiP." provenance.
- _5 value "Modified assertion" provenance.
- _5 value "Modified assertion" provenance.
- _5 value "Modified assertion" provenance.
- _5 value "A major route for FGF signaling is through the mitogen-activated protein kinase (MAPK) pathway. We showed recently that this pathway is important for activation and phosphorylation of Cbfa1/Runx2, an osteoblast-related transcription factor (Xiao, G., Jiang, D., Thomas, P., Benson, M. D., Guan, K., Karsenty, G., and Franceschi, R. T. (2000) J. Biol. Chem. 275, 4453-4459)." provenance.
- _5 value "FGF-2 stimulated osteocalcin mRNA and promoter activity in a dose- and time-dependent manner in MC3T3-E1 preosteoblastic cells. Similar results were obtained in mouse bone marrow stromal cells. This stimulation required Runx2 and its DNA binding site in the osteocalcin promoter" provenance.
- _5 value "Modified assertion" provenance.
- _5 value "Modified assertion" provenance.
- _3 value "Theseresults indicated that the overexpression of CCND2 in squamous cell carcinomalines modulates cell proliferation after induced quiescence and also has apowerful enhancing effect on in vivo aggressive growth behavior." provenance.
- _3 value "In addition, H7, staurosporine, cycloheximide and TGF-beta could suppress MMP-2 production." provenance.
- _4 value "Modified assertion" provenance.
- _6 value "Modified assertion" provenance.
- _4 value "Among the MMPs, MMP-1, -3, -7, and -13 processed CTGF of the complex into the major NH(2)- and COOH-terminal fragments, whereas VEGF(165) was completely resistant to the MMPs." provenance.
- _5 value "On the other hand, elastase and plasmin cleaved both CTGF and VEGF(165) of the complex, but they were completely resistant to ADAMTS4." provenance.
- _3 value "Hsp70 is unabundant in normal physiological situations and strongly induced under oxidative stress. In the present study we show that the chaperoning activity of purified Hsp70 and Hsc70 is minimal under reducing conditions and increases in environments that mimic oxidative stress." provenance.
- _5 value "Our results indicate that murine tissue MA require PKC betaII for phagocytosis of apoptotic cells, which differs from the PKC isoform requirement previously described in MA phagocytosis of other particles, and imply that a crucial action of the PS receptor in this process is PKC betaII activation." provenance.
- _3 value "# Ariadne: Leptin was found to specifically repress RNA levels and enzymatic activity of hepatic stearoyl-CoA desaturase-1 (SCD-1), which catalyzes the biosynthesis of monounsaturated fatty acids. [MolSynthesis]" provenance.
- _3 value "Nicotine-induced caspase-3 activation and Hsp90 alpha expression, as well as suppression of the induction by GA, were also observed in a xeroderma pigmentosum patient-derived cell line, XP2 OS cells." provenance.
- _3 value "In contrast to NE, insulin increases PI 3-kinase activity and phosphorylation of p70 ribosomal S6-kinase." provenance.
- _4 value "It was proposed that NE affects proteolysis indirectly by decreasing cell ATP from activation of uncoupling protein-1 (UCP1)-dependent mitochondrial respiration. This was tested by comparing the effects of NE and fatty acids (which directly activate UCP1)" provenance.
- _2 value "insulin inhibits proteolysis via rapamycin-sensitive activation of p70 ribosomal S6-kinase,whereas the effect of NE appears largely to be a function of decreasing cell ATP content." provenance.
- _3 value "E2 stimulation of S118 phosphorylation was observed within 10 min of its addition" provenance.
- _4 value "From full text: EGF and PMA stimulated S118 phosphorylation" provenance.
- _4 value "The CLP-1 gene promoter is active in different cell types and sequence analysis shows a number of potential binding sites for cardiogenic transcription factors such as Nkx2.5 and GATA-4, indicating a potential role in development." provenance.
- _4 value "These results unveil a new molecular mechanism of signal transduction triggered by integrin engagement where a global mitochondrial metabolic response leads to gene expression rather than apoptosis. Activated RhoA also induced ROS production and up-regulated CL-1 expression." provenance.
- _3 value "We show here the transient activation of the small GTPase Rac, followed by a rise in reactive oxygen species (ROS), as necessary early steps in a signal transduction cascade that lead to NFkappaB activation and collagenase-1 (CL-1)/matrix metalloproteinase-1 production after integrin-mediated cell shape changes." provenance.
- _4 value "We show here the transient activation of the small GTPase Rac, followed by a rise in reactive oxygen species (ROS), as necessary early steps in a signal transduction cascade that lead to NFkappaB activation and collagenase-1 (CL-1)/matrix metalloproteinase-1 production after integrin-mediated cell shape changes." provenance.
- _3 value "The downregulation of Liprin-alpha2 mRNA expression in LNCaP cells was observed after treatment with DHT for 8 and 24 hour." provenance.
- _5 value "the extracellular signal-regulated kinases (ERK1/2) were shown to beinhibited in both phosphorylation status and enzymatic activity afteroverexpression of PTPepsilon." provenance.
- _5 value "over-expression of gamma-synuclein leads to constitutive activation of ERK1/2 and down-regulation of JNK1" provenance.
- _3 value "cAMP-driven PDE4D5 up-regulation in hASMs and suggest a CRE-containing, isoform-specific promoter as the primary mechanism." provenance.
- _5 value "We conclude that MK can act as a growth, survival, and angiogenic factor during tumorigenesis and signals through the ALK receptor." provenance.
- _3 value "The expression of mRNA/protein for caspase-1 and IL-18 in brain homogenates increased progressively at 12 hr to 14 d after HI, whereas IL-1beta peaked at 8 hr. A widespread expression of caspase-1 and IL-18 protein in microglia was found in the HI hemisphere." provenance.
- _3 value "The expression of mRNA/protein for caspase-1 and IL-18 in brain homogenates increased progressively at 12 hr to 14 d after HI, whereas IL-1beta peaked at 8 hr. A widespread expression of caspase-1 and IL-18 protein in microglia was found in the HI hemisphere." provenance.
- _5 value "Hyaluronan-CD44 binding stimulated Ras-Mek1-Mapk pathway, which inturn stimulated MMP-2 secretion in a time and dose dependent manner." provenance.
- _6 value "Hyaluronan-CD44 binding stimulated Ras-Mek1-Mapk pathway, which inturn stimulated MMP-2 secretion in a time and dose dependent manner." provenance.
- _2 value "the invasiveness of QG90 was clearly activated by HA treatment. " provenance.
- _3 value "stella positive nascent germ cells exhibit repression of homeobox genes, which may explain their escape from a somatic cell fate and the retention of pluripotency." provenance.
- _3 value "Accumulating evidence indicates that androgens and the androgen receptor modulate the development and progression of breast adenocarcinoma; however, the precise role and actions remain poorly defined. We examined previously the steroid hormone regulation of 2 known androgen-regulated kallikreins, KLK3 (encoding PSA) and KLK2 (encoding human kallikrein 2 or hK2) in BT-474, T-47D, ZR75-1, MCF-7, MFM-223 and BT-20 human breast cancer cells and found that they were differentially regulated, with the cells showing variable responses to androgen. To determine if this variable response was reflected by differences in androgen receptor, we characterized the expression of androgen receptor in these cells by Western blot analysis and saturation binding analysis. In addition, we sequenced androgen receptor cDNA from each of these cell lines to check whether any androgen receptor mutations were present. The expression of 11 nuclear receptor co-regulatory factors (SRC-1, AIB1, ARA24, ARA54, ARA55, ARA70, ARA160, FHL2, PDEF, NCoR1, SMRT) was compared in these cell lines by semi-quantitative RT-PCR to determine if the pattern of receptor co-activators or -repressors expressed in these cells might explain the differential regulation of KLK2 and KLK3. The levels of androgen receptor varied among the cell lines, but did not correlate with hK2 and PSA secretion determined previously. No mutations within the coding regions of the receptor were detected. With the exception of receptor expressed by MCF-7 cells, the polymorphic CAG repeat length was in the normal range. Every breast cancer cell line exhibited a distinct expression pattern of the nuclear receptor co-regulators examined raising the possibility that the relative levels of these co-activators/-repressors might differentially modulate androgen receptor transcriptional activity within the promoter/enhancer region of KLK2 and KLK3 of these cells." provenance.
- _3 value "an inhibition of insulin receptor (IR) mRNA levels and insulin binding by aldosterone this inhibition of the insulin response by aldosterone is mediated by a downregulation of the levels of mineralocorticoid receptors (MRs) (50% decrease) and their mRNA (50% decrease)" provenance.
- _2 value "an inhibition of insulin receptor (IR) mRNA levels and insulin binding by aldosterone this inhibition of the insulin response by aldosterone is mediated by a downregulation of the levels of mineralocorticoid receptors (MRs) (50% decrease) and their mRNA (50% decrease)" provenance.
- _4 value "Cardiac ankyrin repeat protein (CARP), glutathione peroxidase (Gpx1), and genes which participate in the formation of extracellular matrix including decorin, TSC-36, Magp2, Osf2, and SPARC are upregulated in CSQ mouse hearts at 7 and 13 weeks of age compared to those of non-transgenic littermates." provenance.
- _4 value "Cardiac ankyrin repeat protein (CARP), glutathione peroxidase (Gpx1), and genes which participate in the formation of extracellular matrix including decorin, TSC-36, Magp2, Osf2, and SPARC are upregulated in CSQ mouse hearts at 7 and 13 weeks of age compared to those of non-transgenic littermates." provenance.
- _4 value "Cardiac ankyrin repeat protein (CARP), glutathione peroxidase (Gpx1), and genes which participate in the formation of extracellular matrix including decorin, TSC-36, Magp2, Osf2, and SPARC are upregulated in CSQ mouse hearts at 7 and 13 weeks of age compared to those of non-transgenic littermates." provenance.
- _4 value "Several genes are downregulated at 13 weeks, including SR Ca2+-ATPase (SERCA2) and adenine nucleotide translocase 1 (Ant1) genes." provenance.
- _4 value "Several genes are downregulated at 13 weeks, including SR Ca2+-ATPase (SERCA2) and adenine nucleotide translocase 1 (Ant1) genes." provenance.
- _5 value "In the rat pineal gland, prominent expression of serine protease inhibitor 3 (SPI-3) mRNA is seen after systemic injection of lipopolysaccharide. The up-regulation of SPI-3 mRNA expression is also confirmed by northern blotting. Most SPI-3 mRNA-positive cells simultaneously express synaptophysin, a marker for pinealocytes, but not glial fibrillary acidic protein, a marker for astrocytes. This indicates that SPI-3 mRNA-positive cells are pinealocytes. Almost all SPI-3 mRNA-positive cells also showed translocation of the signal transducers and activators of transcription 3 (STAT3) into nuclei after lipopolysaccharide injection. These data support previous in vitro results that SPI-3 expression is induced in a STAT3-mediated manner. In addition, the expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs, but not of interleukin 6 receptor mRNA, was up-regulated after systemic lipopolysaccharide treatment. Because these receptors are upstream of STAT3, the present results suggest that cytokines such as LIF and/or CNTF induce SPI-3 expression via STAT3 in the pineal gland in response to inflammatory stimulus. We conclude that although the functional consequences of SPI-3 in the pineal gland during systemic inflammation are unknown, SPI-3 may have a crucial role in preventing some degenerative proteolysis induced by inflammatory stimuli." provenance.
- _5 value "In the rat pineal gland, prominent expression of serine protease inhibitor 3 (SPI-3) mRNA is seen after systemic injection of lipopolysaccharide. The up-regulation of SPI-3 mRNA expression is also confirmed by northern blotting. Most SPI-3 mRNA-positive cells simultaneously express synaptophysin, a marker for pinealocytes, but not glial fibrillary acidic protein, a marker for astrocytes. This indicates that SPI-3 mRNA-positive cells are pinealocytes. Almost all SPI-3 mRNA-positive cells also showed translocation of the signal transducers and activators of transcription 3 (STAT3) into nuclei after lipopolysaccharide injection. These data support previous in vitro results that SPI-3 expression is induced in a STAT3-mediated manner. In addition, the expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs, but not of interleukin 6 receptor mRNA, was up-regulated after systemic lipopolysaccharide treatment. Because these receptors are upstream of STAT3, the present results suggest that cytokines such as LIF and/or CNTF induce SPI-3 expression via STAT3 in the pineal gland in response to inflammatory stimulus. We conclude that although the functional consequences of SPI-3 in the pineal gland during systemic inflammation are unknown, SPI-3 may have a crucial role in preventing some degenerative proteolysis induced by inflammatory stimuli." provenance.
- _3 value "In the rat pineal gland, prominent expression of serine protease inhibitor 3 (SPI-3) mRNA is seen after systemic injection of lipopolysaccharide. The up-regulation of SPI-3 mRNA expression is also confirmed by northern blotting. Most SPI-3 mRNA-positive cells simultaneously express synaptophysin, a marker for pinealocytes, but not glial fibrillary acidic protein, a marker for astrocytes. This indicates that SPI-3 mRNA-positive cells are pinealocytes. Almost all SPI-3 mRNA-positive cells also showed translocation of the signal transducers and activators of transcription 3 (STAT3) into nuclei after lipopolysaccharide injection. These data support previous in vitro results that SPI-3 expression is induced in a STAT3-mediated manner. In addition, the expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs, but not of interleukin 6 receptor mRNA, was up-regulated after systemic lipopolysaccharide treatment. Because these receptors are upstream of STAT3, the present results suggest that cytokines such as LIF and/or CNTF induce SPI-3 expression via STAT3 in the pineal gland in response to inflammatory stimulus. We conclude that although the functional consequences of SPI-3 in the pineal gland during systemic inflammation are unknown, SPI-3 may have a crucial role in preventing some degenerative proteolysis induced by inflammatory stimuli." provenance.
- _3 value "In the rat pineal gland, prominent expression of serine protease inhibitor 3 (SPI-3) mRNA is seen after systemic injection of lipopolysaccharide. The up-regulation of SPI-3 mRNA expression is also confirmed by northern blotting. Most SPI-3 mRNA-positive cells simultaneously express synaptophysin, a marker for pinealocytes, but not glial fibrillary acidic protein, a marker for astrocytes. This indicates that SPI-3 mRNA-positive cells are pinealocytes. Almost all SPI-3 mRNA-positive cells also showed translocation of the signal transducers and activators of transcription 3 (STAT3) into nuclei after lipopolysaccharide injection. These data support previous in vitro results that SPI-3 expression is induced in a STAT3-mediated manner. In addition, the expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs, but not of interleukin 6 receptor mRNA, was up-regulated after systemic lipopolysaccharide treatment. Because these receptors are upstream of STAT3, the present results suggest that cytokines such as LIF and/or CNTF induce SPI-3 expression via STAT3 in the pineal gland in response to inflammatory stimulus. We conclude that although the functional consequences of SPI-3 in the pineal gland during systemic inflammation are unknown, SPI-3 may have a crucial role in preventing some degenerative proteolysis induced by inflammatory stimuli." provenance.
- _3 value "In the rat pineal gland, prominent expression of serine protease inhibitor 3 (SPI-3) mRNA is seen after systemic injection of lipopolysaccharide. The up-regulation of SPI-3 mRNA expression is also confirmed by northern blotting. Most SPI-3 mRNA-positive cells simultaneously express synaptophysin, a marker for pinealocytes, but not glial fibrillary acidic protein, a marker for astrocytes. This indicates that SPI-3 mRNA-positive cells are pinealocytes. Almost all SPI-3 mRNA-positive cells also showed translocation of the signal transducers and activators of transcription 3 (STAT3) into nuclei after lipopolysaccharide injection. These data support previous in vitro results that SPI-3 expression is induced in a STAT3-mediated manner. In addition, the expression of ciliary neurotrophic factor receptor (CNTFR) and leukemia inhibitory factor receptor (LIFR) mRNAs, but not of interleukin 6 receptor mRNA, was up-regulated after systemic lipopolysaccharide treatment. Because these receptors are upstream of STAT3, the present results suggest that cytokines such as LIF and/or CNTF induce SPI-3 expression via STAT3 in the pineal gland in response to inflammatory stimulus. We conclude that although the functional consequences of SPI-3 in the pineal gland during systemic inflammation are unknown, SPI-3 may have a crucial role in preventing some degenerative proteolysis induced by inflammatory stimuli." provenance.
- _4 value "Previous in vitro studies have shown that growth hormone (GH) can inhibit PPARalpha-dependent gene expression by down-regulation of PPARalpha expression and by a novel inhibitory cross-talk involving the GH-activated transcription factor STAT5b. ...A corresponding increase in mRNA, was observed in the STAT5b-deficient mice, suggesting a transcriptional mechanism for the observed increases." provenance.
- _5 value "Previous in vitro studies have shown that growth hormone (GH) can inhibit PPARalpha-dependent gene expression by down-regulation of PPARalpha expression and by a novel inhibitory cross-talk involving the GH-activated transcription factor STAT5b. ...A corresponding increase in mRNA, was observed in the STAT5b-deficient mice, suggesting a transcriptional mechanism for the observed increases." provenance.
- _7 value "# Ariadne: Apparently all D- type cyclins can block MEF2 activity as cotransfection of cyclin D1, D2, or D3 together with cdk4 blocked the ability of exogenous MEF2C to activate expression of the MEF2x3LUC reporter in 10T1/2 cells (Fig. 1 C, cf. lane 2 with lanes 3,4,5). [Regulation] # Ariadne: In addition, because it is known that GRIP-1 can rapidly exchange in and out of the punctate nuclear structures when bound to steroid hormone receptors ( Schaufele et al. 2000 ), it seems possible that the GRIP-1-MEF2 complex may similarly diffuse in and out of these structures. [Binding] Prior work has indicated that D-type cyclin-cdk4 complexes, which are only active in proliferating cells, can suppress the skeletal muscle differentiation program in proliferating myoblasts. We have found that cyclin D-cdk activity blocks the association of MEF2C with the coactivator protein GRIP-1 and thereby inhibits the activity of MEF2. Our findings indicate that cyclin D-cdk4 activity represses skeletal muscle differentiation in proliferating cells by blocking the association of MEF2 with the coactivator GRIP-1 and concomitantly disrupts the association of these factors with punctate nuclear subdomains within the cell." provenance.
- _6 value "Our findings indicate that cyclin D-cdk4 activity represses skeletal muscle differentiation in proliferating cells by blocking the association of MEF2 with the coactivator GRIP-1 and concomitantly disrupts the association of these factors with punctate nuclear subdomains within the cell." provenance.
- _5 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _4 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _4 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _6 value "The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts" provenance.
- _4 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _4 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _6 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _6 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _6 value "In this study, cAMP-elevating agents such as isoproterenol, prostaglandin E(2), CGS-21680 (an adenosine A(2a) receptor agonist), the type IV phosphodiesterase inhibitor RO 20-1724, the adenylate cyclase activator forskolin, and the Gs-protein activator cholera toxin all inhibited LT biosynthesis and 5-LO translocation to the nucleus in cytokine-primed human PMN" provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _3 value "Specifically, expression of Cyp2b9, Cyp3a16, Cyp4a14, and Gstt2 was increased, whereas expression of Cyp1a2, Cyp2c22, Cyp2c29, Cyp2c40, Gstm3, and Gstm6 was suppressed in diabetes." provenance.
- _6 value "This suggests that PKC-alpha is required for GRK2 and GRK3 translocation from the cytosol to the membrane, where GRK can inactivate ORL1 and mu opioid receptors" provenance.
- _3 value "Both statins reduced ox-LDL-mediated activation of the redox-sensitive nuclear factor-kappaB (NF-kappaB) but not AP-1." provenance.
- _4 value "LOX-1 activation also plays an important role in monocyte adhesion to endothelial cells" provenance.
- _3 value "Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced expression of LOX-1 as well as adhesion molecules" provenance.
- _3 value "Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced expression of LOX-1 as well as adhesion molecules" provenance.
- _3 value "Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced expression of LOX-1 as well as adhesion molecules" provenance.