Matches in Nanopublications for { ?s <http://www.w3.org/ns/prov#value> ?o ?g. }
- _3 value "Ha-Ras cooperates with transforming growth factor beta (TGFbeta) to cause epithelial mesenchymal transition (EMT) characterized by spindle-like cell morphology, loss of epithelial markers, and induction of mesenchymal markers." provenance.
- _3 value "In addition to oncogenic Ras (Oft et al., 1996), hepatocyte growth factor (HGF)/scatter factor (SF), fibroblast growth factor (FGF), and TGF alone induce mesenchymal features in diverse epithelial cell systems (Brinkmann et al., 1995; Piek et al., 1999; Thiery and Chopin, 1999)." provenance.
- _3 value "Raf/mitogen-activated protein kinase (MAPK) is required for EMT, whereas activation of phosphatidylinositol 3-kinase (PI3K) causes scattering and protects from TGFbeta-induced apoptosis." provenance.
- _4 value "The statement below comes from the actual article" provenance.
- _4 value "HDL binding to SR-BI caused a reversible increase in intracellular ceramide levels from 97 +/- 14 pmol/mg of protein to 501 +/- 21 pmol/mg of protein. " provenance.
- _5 value "administration of a diet supplemented with high levels of cholesterol increases the expression of Cyp7a1, bile acid synthesis and excretion in wild-type mice, but not in Lxra null or Lxrb null mice" provenance.
- _5 value "administration of a diet supplemented with high levels of cholesterol increases the expression of Cyp7a1, bile acid synthesis and excretion in wild-type mice, but not in Lxra null or Lxrb null mice" provenance.
- _4 value "consistent with this proposal, all Lxr target genes encode proteins that have major roles in controlling cholesterol and or fatty acid homeostasis in a number of tissues including the liver, intestine, macrophages and possibly adipose tissue primary bile acids, such as CDCA or CA, bind to Fxr in vitro, this interaction occurs at physiological levels of the bile acids this interaction results in recruitment of coactivators to the liganded Fxr, and that there is a subsequent increase in the transcription of target genes Fxr transcripts are restricted to the liver, kidney, intestine [all involved in cholesterol/bile acid metabolism], colon, and adrenals" provenance.
- _4 value "many, but not all, non-steroidal nuclear receptors are thought to be pre-bound to the HRE in a complex with corepressor proteins entry of the ligand into the LBD initiates changes int he conformation of the receptor that results in loss of corepressor proteins, recruitment of coactivator proteins and increased transcription identified oxysterols, such as 24S,25-epoxycholesterol, 20S-,22R-,24S- and 27-hydroxycholesterol, as activators of of Lxr" provenance.
- _4 value "many, but not all, non-steroidal nuclear receptors are thought to be pre-bound to the HRE in a complex with corepressor proteins entry of the ligand into the LBD initiates changes int he conformation of the receptor that results in loss of corepressor proteins, recruitment of coactivator proteins and increased transcription identified oxysterols, such as 24S,25-epoxycholesterol, 20S-,22R-,24S- and 27-hydroxycholesterol, as activators of of Lxr" provenance.
- _4 value "primary bile acids, such as chenodeoxycholic acid and cholic acid as activators of Fxr" provenance.
- _4 value "D6d activity is induced by peroxisome proliferators and by the supplementation of insulin to diabetic rats it is also highly suppressed by dietary Pufa, indicating that these enzymes are involved in feedback regulation in the production of AA, EPA and DHA" provenance.
- _3 value "the hepatic expression of both desaturases was downregulated by dietary PUFA, which were reported to suppress Srebf1c gene expression sustained expression of hepatic nuclear Srebf1c protein in the transgenic mice abolished the PUFA suppression of both desaturases" provenance.
- _6 value "Erk phosphorylates serine residues in the linker regions of Smad1 (Kretzschmar et al., 1997), Smad2 and Smad3 (Kretzschmar et al., 1999), and substitution of these serines by negatively charged residues inhibits nuclear translocation of Smads and thus signalling." provenance.
- _5 value "Finally, I-Smads are constitutively imported to the nucleus and are exported to the cytoplasm in response to TGF-b or BMP signalling (Itoh et al., 1998; Itoh et al., 2001)." provenance.
- _6 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _7 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _5 value "Phosphorylation of the C-terminal serine residues in R-Smads by type I receptor kinases is a crucial step in TGF-b family signalling (Abdollah et al., 1997; Macias-Silva et al., 1996; Souchelnytskyi et al., 1997). The two most C-terminal serine residues become phosphorylated and, together with a third, non-phosphorylated serine residue, form an evolutionarily conserved SSXS motif in all R-Smads.... TGF-b and activin receptors phosphorylate Smad2 and Smad3, and BMP receptors phosphorylate Smad1, Smad5 and Smad8 (Chen et al., 1998) (Fig. 1). The consequence of R-Smad phosphorylation is the formation of oligomeric complexes with the Co-Smad, Smad4." provenance.
- _6 value "These proteins signal by stimulating formation of specific heteromeric complexes of type I and type II serine/threonine kinase receptors. The type II receptors are encoded by five known mammalian genes, bind to ligands, and phosphorylate and activate the type I receptors, of which there are seven mammalian members (Fig. 1)." provenance.
- _6 value "These proteins signal by stimulating formation of specific heteromeric complexes of type I and type II serine/threonine kinase receptors. The type II receptors are encoded by five known mammalian genes, bind to ligands, and phosphorylate and activate the type I receptors, of which there are seven mammalian members (Fig. 1)." provenance.
- _3 value "Lipin is the product of the gene that is mutated in fatty liver dystrophy mice which exhibit several phenotypic abnormalities including hyperlipidemia, defects in adipocyte differentiation, impaired glucose tolerance, and slow growth" provenance.
- _3 value "Lipin is the product of the gene that is mutated in fatty liver dystrophy mice which exhibit several phenotypic abnormalities including hyperlipidemia, defects in adipocyte differentiation, impaired glucose tolerance, and slow growth" provenance.
- _5 value "Thus, lipin represents a target of the mTOR pathway, and potentially links this nutrient-sensing pathway to adipocyte development." provenance.
- _3 value "incubating adipocytes with insulin decreases the electrophoretic mobility and stimlulated the phosphorylation of both Ser and Thr residues in lipin" provenance.
- _3 value "incubating adipocytes with insulin decreases the electrophoretic mobility and stimlulated the phosphorylation of both Ser and Thr residues in lipin" provenance.
- _5 value "the effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase" provenance.
- _5 value "the effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase" provenance.
- _5 value "the effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase" provenance.
- _5 value "the effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase" provenance.
- _5 value "the effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase" provenance.
- _7 value "title := \"Insulin-stimulated phosphorylation of lipin mediated by the mammalian target of rapamycin.\" Incubating adipocytes with insulin decreased the electrophoretic mobility and stimulated the phosphorylation of both Ser and Thr residues in lipin. The effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase, and by rapamycin, a specific inhibitor of the mammalian target of rapamcyin (mTOR)." provenance.
- _5 value "title := \"Insulin-stimulated phosphorylation of lipin mediated by the mammalian target of rapamycin.\" Incubating adipocytes with insulin decreased the electrophoretic mobility and stimulated the phosphorylation of both Ser and Thr residues in lipin. The effects of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase, and by rapamycin, a specific inhibitor of the mammalian target of rapamcyin (mTOR)." provenance.
- _3 value "Previously, it was found that hypertonicity rapidly causes nuclear translocation and phosphorylation of TonEBP/OREBP and, more slowly, increases TonEBP/OREBP abundance." provenance.
- _3 value "Previously, it was found that hypertonicity rapidly causes nuclear translocation and phosphorylation of TonEBP/OREBP and, more slowly, increases TonEBP/OREBP abundance." provenance.
- _4 value "Previously, it was found that hypertonicity rapidly causes nuclear translocation and phosphorylation of TonEBP/OREBP and, more slowly, increases TonEBP/OREBP abundance." provenance.
- _5 value "The activity at 500 mosmol/kg was reduced by herbimycin, a tyrosine kinase inhibitor and by 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole, a protein kinase CK2 inhibitor." provenance.
- _4 value "CD36 recognizes a broad variety of ligands including OxLDL,11,20 anionic phospholipids,21 apoptotic cells,22 thrombospondin (TSP),23 collagen,24 Plasmodium falciparum-infected erythrocytes, 25 and long-chain fatty acids.18" provenance.
- _4 value "Induction of CD36 by OxLDL is due to its ability to activate the transcription factor PPAR-? (peroxisome proliferator activated receptor-?).33,34" provenance.
- _3 value "There was a significant decrease in binding and uptake of OxLDL in peritoneal macrophages of null mice as compared with those from control mice." provenance.
- _5 value "Besides being activated by ligand binding, the EGFR can be transactivated by a growing number of different pathways, including G-protein-coupled receptors (GPCRs), cytokine receptors, ion channels, integrins, and other RTKs.37" provenance.
- _5 value "ASK1, a MAP kinase kinase kinase mediating the TNF-alpha signal has been identified as a thioredoxin binding protein. Thioredoxin shows an inhibitory effect on the TNF-alpha induced activation of ASK1" provenance.
- _3 value "Elastase treatment resulted in increases in TUNEL-positive cells in the lungs of wild-type, PPE-treated mice (Fig. 4).Brown staining was detected in cells in the alveolar wall but was predominantly found in the cytoplasm of macrophages." provenance.
- _4 value "Fibrates are widely used...in lowering plasma triglyceride and cholesterol levels. The decrease of triglyceride by the drugs is thought to be the result of induction of lipoprotein lipase activity in peripheral tissues and the decrease of apolipoprotein C-III gene expression in liver." provenance.
- _4 value "Fibrates are widely used...in lowering plasma triglyceride and cholesterol levels. The decrease of triglyceride by the drugs is thought to be the result of induction of lipoprotein lipase activity in peripheral tissues and the decrease of apolipoprotein C-III gene expression in liver." provenance.
- _3 value "Fibrates down regulate genes for ApoA-I , apoA-AIV, hepatic lipase, and lecithin:cholesterol acyltransferase. On the other hand, fibrates up-regulate genes for lipoprotein lipase, acyl-CoA synthethase and several enzymes related to b-oxidation, such as acyl-CoA oxidase." provenance.
- _3 value "Fibrates down regulate genes for ApoA-I , apoA-AIV, hepatic lipase, and lecithin:cholesterol acyltransferase. On the other hand, fibrates up-regulate genes for lipoprotein lipase, acyl-CoA synthethase and several enzymes related to b-oxidation, such as acyl-CoA oxidase." provenance.
- _3 value "Fibrates down regulate genes for ApoA-I , apoA-AIV, hepatic lipase, and lecithin:cholesterol acyltransferase. On the other hand, fibrates up-regulate genes for lipoprotein lipase, acyl-CoA synthethase and several enzymes related to b-oxidation, such as acyl-CoA oxidase." provenance.
- _3 value "Fibrates down regulate genes for ApoA-I , apoA-AIV, hepatic lipase, and lecithin:cholesterol acyltransferase. On the other hand, fibrates up-regulate genes for lipoprotein lipase, acyl-CoA synthethase and several enzymes related to b-oxidation, such as acyl-CoA oxidase." provenance.
- _5 value "CGRP and Adm potentiated the expression of HRG-1, thus inhibiting the activity of MAPK" provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _3 value "(From full text) Figure 3. Identification of E2F1 and E2F4 binding sites on human promoters (p<0.01). " provenance.
- _7 value "stimulation of CD95 receptors, with either agonistic antibody or CD95 ligand, resulted in the activation of caspase-8, which in turn processed caspase-3" provenance.
- _4 value "Fig. 4 A shows that KJ1-26 + CD4 + T cells from the Ld-nOVA recipients expressed lower levels of CD62L and CD45RB and a higher level of CD44 than KJ1-26 + CD4 + T cells from the nontransgenic recipients." provenance.
- _4 value "The binding of AP-1 to the relevant promoter sequence depended on the presence of STAT4. STAT4 bound with c-Jun, and a phosphorylated c-Jun-STAT4 complex most efficiently interacted with the AP-1-relevant promoter sequence. Enhanced cobinding of STAT4 and c-Jun to the AP-1 sequence was also observed when activated lymph node T cells were exposed to IL-12 plus IL-18. These results show that STAT4 up-regulates AP-1-mediated IFN-gamma promoter activation without directly binding to the promoter sequence, providing a mechanistic explanation for IL-12/IL-18-induced synergistic enhancement of IFN-gamma gene expression." provenance.
- _4 value "ELISA analysis of whole lung levels of IP-10/CXCL10 and MIG/CXCL9 in both groups of mice revealed that both non-ELR CXC chemokines were significantly elevated in CXCR2-/- mice compared with those in CXCR2+/+ mice (Fig. 8Go)." provenance.
- _4 value "HEF1 production increases levels of mRNA transcripts encoding proteins that are associated with motility, cell transformation and invasiveness, including several metalloproteinases, MLCK, p160ROCK and ErbB2. Upregulation of such proteins suggests mechanisms through which misregulation of HEF1 may be involved in cancer progression." provenance.
- _3 value "HEF1 production rapidly induces changes in cellular morphology and motility, enhancing cell speed and haptotaxis towards fibronectin in a process partially dependent on intact ERK and p38 MAPK signaling pathways" provenance.
- _4 value "Hef1 production increases levels of mRNA transcripts encoding proteins that are associated with motility, cell transformation and invasiveness, including several metalloproteinases, MLCK, p160ROCK, and ErbB2" provenance.
- _5 value "Modified assertion" provenance.
- _3 value "Hyperoxia-induced mRNA levels of NAD(P)H:quinone oxidoreductase 1 (NQO1), glutathione-S-transferase (GST)-Ya and -Yc subunits, UDP glycosyl transferase (UGT), glutathione peroxidase-2 (GPx2), and heme oxygenase-1 (HO-1) were significantly lower in Nrf2-/- mice compared with Nrf2+/+ mice." provenance.
- _3 value "Hyperoxia-induced mRNA levels of NAD(P)H:quinone oxidoreductase 1 (NQO1), glutathione-S-transferase (GST)-Ya and -Yc subunits, UDP glycosyl transferase (UGT), glutathione peroxidase-2 (GPx2), and heme oxygenase-1 (HO-1) were significantly lower in Nrf2-/- mice compared with Nrf2+/+ mice." provenance.
- _3 value "P4 increased PGIS expression in the uterine, mammary, omental, and renal artery VSM, and E2beta increased PGIS expression in the uterine and omental artery VSM" provenance.
- _5 value "Caveolin-1 is a substrate for nonreceptor tyrosine kinases including Src, Fyn, and Abl." provenance.
- _4 value "Inhibitory effect of EGF and OSM on cell proliferation was completely blocked by MEK1 inhibitor (PD98059)." provenance.
- _4 value "Simultaneous inhibition of PDE5, 6, and 9 (zaprinast)," provenance.
- _4 value "nonselective inhibition of PDE by pentoxifylline suppressed LPS-mediated secretion of IL-6 and TNF-alpha" provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.
- _3 value "Understanding the response of innate immune cells to pathogens may provide insights to host defenses and the tactics used by pathogens to circumvent these defenses. We used DNA microarrays to explore the responses of human macrophages to a variety of bacteria. Macrophages responded to a broad range of bacteria with a robust, shared pattern of gene expression. The shared response includes genes encoding receptors, signal transduction molecules, and transcription factors. This shared activation program transforms the macrophage into a cell primed to interact with its environment and to mount an immune response. Further study revealed that the activation program is induced by bacterial components that are Toll-like receptor agonists, including lipopolysaccharide, lipoteichoic acid, muramyl dipeptide, and heat shock proteins. Pathogen-specific responses were also apparent in the macrophage expression profiles. Analysis of Mycobacterium tuberculosis-specific responses revealed inhibition of interleukin-12 production, suggesting one means by which this organism survives host defenses. These results improve our understanding of macrophage defenses, provide insights into mechanisms of pathogenesis, and suggest targets for therapeutic intervention." provenance.