Only in Titles

           Search results for: NF kB reporter (Luc) HEK293 Cell line   

paperclip

#29534536   // Save this To Up

Lung Cancer Chemopreventive Activity of Patulin Isolated from Penicillium vulpinum.

Lung cancer is the most lethal form of cancer in the world. Its development often involves an overactivation of the nuclear factor kappa B (NF-κB) pathway, leading to increased cell proliferation, survival, mobility, and a decrease in apoptosis. Therefore, NF-κB inhibitors are actively sought after for both cancer chemoprevention and therapy, and fungi represent an interesting unexplored reservoir for such molecules. The aim of the present work was to find naturally occurring lung cancer chemopreventive compounds by investigating the metabolites of , a fungus that grows naturally on dung. was cultivated in Potato Dextrose Broth and extracted with ethyl acetate. Bioassay-guided fractionation of this extract was performed by measuring NF-κB activity using a HEK293 cell line transfected with an NF-κB-driven luciferase reporter gene. The mycotoxin patulin was identified as a nanomolar inhibitor of TNF-α-induced NF-κB activity. Immunocytochemistry and Western blot analyses revealed that its mechanism of action involved an inhibition of p65 nuclear translocation and was independent from the NF-κB inhibitor α (IκBα) degradation process. Enhancing its interest in lung cancer chemoprevention, patulin also exhibited antiproliferative, proapoptotic, and antimigration effects on human lung adenocarcinoma cells through inhibition of the Wnt pathway.

2030 related Products with: Lung Cancer Chemopreventive Activity of Patulin Isolated from Penicillium vulpinum.

Advanced lung cancer and Lung cancer tissue array, Lung cancer high density High density lung cancer Lung cancer tissue array Lung cancer test tissue a Lung cancer tissue array, Lung cancer survey tissue Multiple lung cancer tiss High density lung cancer Lung cancer tissue array, Top 4 types of cancer (co

Related Pathways

paperclip

#28690191   // Save this To Up

Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate can suppress MCP-1 expression by inhibiting p38 MAP kinase and NF-κB in LPS-stimulated differentiated THP-1 cells.

Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate (MHAT) is an O-methyl ester of javamide-II showing strong anti-inflammatory activity. Therefore, in this study, MHAT was chemically synthesized, and its effects on p38 MAP kinase, NF-κB, and monocyte chemotactic factor-1 (MCP-1) expression were investigated in LPS-stimulated differentiated THP-1 cells. MHAT inhibited p38 MAP kinase with an IC of 12μM, and the inhibition was supported by an in silico model showing that its binding to p38 MAP kinase was stronger than that of SB203580. At the concentration of 20μM, the p38 inhibition reduced ATF-2 phosphorylation by 55% (P < 0.05). Additionally, MHAT inhibited NF-κB (p65) phosphorylation by 30% (P < 0.05) at the same concentration, suggesting that MHAT was able to reduce NF-κB transcriptional activity. This supposition was confirmed by the NF-κB reporter assay, demonstrating that MHAT (20μM) could suppress NF-κB transcriptional activity by 29% (P < 0.05) in the NF-κB reporter (Luc)-HEK293 cell line. As expected, the treatment with MHAT (5-40μM) significantly inhibited MCP-1 mRNA expression by 9-73% (P < 0.05) and the production of MCP-1 protein by 10-70% (P < 0.05) in the THP-1 cells. Furthermore, MHAT was found to inhibit RANTES expression as well in the same THP-1 cells, supporting its purported inhibition of p38 MAP kinase and NF-κB. All these data suggest that MHAT is a potent compound that can inhibit MCP-1 production by suppressing p38 kinase/ATF-2 phosphorylation and NF-κB in the differentiated THP-1 cells.

2222 related Products with: Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate can suppress MCP-1 expression by inhibiting p38 MAP kinase and NF-κB in LPS-stimulated differentiated THP-1 cells.

Rabbit Anti-p38MAPK MAPK1 1-Benzyl-4-[(6-benzyloxy- D,L-7-Aza-3-indolylglycin 3-Amino-1-methyl-5H-pyrid Sf21 insect cells (3R)-3-[[2-(1,3-Benzodiox 1-Acetyl-2,3-dihydro-2-me Rabbit Anti-p38MAPK MAPK1 (1R,3S)-1-(1,3-Benzodioxo Canine Red Blood Cells 10 Rabbit Anti-p38MAPK MAPK1 Rabbit Anti-p38MAPK MAPK1

Related Pathways

paperclip

#28650473   // Save this To Up

Testes-specific protease 50 promotes cell proliferation via inhibiting activin signaling.

Testes-specific protease 50 (TSP50), a novelly identified oncogene, has the capacity to induce cell proliferation, cell invasion and tumor growth. Further studies indicated that CAGA-luc (an activin-responsive reporter construct) reporter activity could be significantly suppressed by TSP50 overexpression, implying that the activin signaling may participate in TSP50-mediated cell proliferation. Here, we reported that TSP50 had an inhibitory effect on activin signaling. Mechanistic studies revealed that TSP50 could interact with ActRIIA, inhibit activin typeIreceptor (ActRIB) phosphorylation, repress Smad2/3 nuclear accumulation and finally promote cell proliferation by reducing the expression of activin signal target gene p27. Additionally, we found that ActRIB activation could reverse TSP50-mediated cell proliferation and tumor growth. Furthermore, analysis of human breast cancer specimens by immunohistochemistry indicated that TSP50 expression was negatively related to p-Smad2/3 and p27 protein levels. Most importantly, breast cancer diagnosis-related indicators such as tumor size, tumor grade, estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER-2) levels, were correlated well with TSP50/p-Samd2/3 and TSP50/p27 expression status. Thus, our studies revealed a novel regulatory mechanism underlying TSP50-induced cell proliferation and provided a new favorable intervention target for the treatment of breast cancer.

2669 related Products with: Testes-specific protease 50 promotes cell proliferation via inhibiting activin signaling.

T-Cell Receptor Signaling CellQuanti Blue™ Cell V Rat monoclonal anti mouse Marker Gene™ Non-Radioa Hygromycin B, EvoPure™, RubyGlowTM Luminescent Ce Competent Cells for Cloni Cell Meter™ Cell Viabil CellQuanti-MTT™ Cell Vi Epidermal Growth Factor ( T-cell proliferation grad TCHII T cell proliferatio

Related Pathways

paperclip

#27264312   // Save this To Up

Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-κB inhibition.

C/EBP homologous protein (CHOP) is a transcription factor that is activated at multiple levels during ER stress and plays an important role in ER stress-induced apoptosis. In this study we identified a novel CHOP activator, and further investigated its potential to be a therapeutic agent for human lung cancer.

1115 related Products with: Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-κB inhibition.

Lung cancer tissue array, Anti beta3 AR Human, Poly Lung cancer tissue array High density (208 cores), Lung cancer tissue array, Macrophage Colony Stimula Lung cancer test tissue a Lung cancer tissue array Lung cancer and adjacent Lung non small cell cance Lung cancer survey tissue Lung cancer tissue array,

Related Pathways

paperclip

#23529230   // Save this To Up

[Functional role of protein kinase D1 in Aspergillus fumigatus-induced activation of nuclear factor-κB signal pathway and transcription].

To explore the functional role of protein kinase D1 (PKD1) in the activation of nuclear factor-κB (NF-κB) signal pathway and NF-κB transcription mediated by Aspergillus fumigatus.

1697 related Products with: [Functional role of protein kinase D1 in Aspergillus fumigatus-induced activation of nuclear factor-κB signal pathway and transcription].

IGF-1R Signaling Phospho- PathwayReady™ MAP Kinas p130Cas-associated protei NF-kB II Phospho-Specific Bovine prolactin-induced PathwayReady™ JAK STAT AKT PKB Signaling Phospho ErbB Her Signaling Phosph Native Pig Intrinsic Fact Goat Anti-Human Tissue Fa TGF-Beta Signaling Phosph to FAPβ (Fibroblast Act

Related Pathways

paperclip

#17522215   // Save this To Up

Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.

Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority of the human adult population in the world. TLR2, a member of the Toll-like receptor (TLR) family, has been implicated in the immune responses to different viruses including members of the herpesvirus family, such as human cytomegalovirus, herpes simplex virus type 1, and varicella-zoster virus. In this report, we demonstrate that infectious and UV-inactivated EBV virions lead to the activation of NF-kappaB through TLR2 using HEK293 cells cotransfected with TLR2-expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2) by EBV was not enhanced by the presence of CD14. The effect of EBV was abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2 antibodies or by preincubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human monocytes induced the release of MCP-1 (monocyte chemotactic protein 1), and the use of small interfering RNA targeting TLR2 significantly reduced such a chemokine response to EBV. Taken together, these results indicate that TLR2 may be an important pattern recognition receptor in the immune response directed against EBV infection.

1230 related Products with: Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.

Human Epstein-Barr Virus Recombinant Human Papillo Recombinant Human IL-6 anti RhoD human antigen I Epstein Barr Virus VCA Ig Recombinant Human Flt3-Li Recombinant Human IL-15 Recombinant Viral Antige Viral antibodies, anti-R Recombinant Human IL-4 Epstein Barr Virus VCA Ig Recombinant Human IL-1 al

Related Pathways

paperclip

#12807870   // Save this To Up

Toll-like receptor (TLR) 2 and TLR5, but not TLR4, are required for Helicobacter pylori-induced NF-kappa B activation and chemokine expression by epithelial cells.

Infection with Helicobacter pylori, a Gram-negative, microaerophilic, flagellated bacteria that adheres to human gastric mucosa, is strongly associated with gastric ulcers and adenocarcinoma. The mechanisms through which gastric epithelial cells recognize this organism are unclear. In this study we evaluated the interactions between the Toll-like receptors (TLRs) and H. pylori-mediated NF-kappa B activation and the induction of chemokine mRNA expression. By reverse transcriptase-PCR we determined that MKN45 gastric epithelial cells express low but detectable amounts of TLR2, -4, and -5 but no MD-2. To determine which, if any, TLRs may play a role in the response of epithelial cells to H. pylori, HEK293 cells were cotransfected with the NF-kappa B-Luc reporter, CD14 and MD2 expression plasmids, and expression plasmids for TLR2, TLR4, or TLR5. Infection of the cultures with H. pylori (strain 26695) induced NF-kappa B activity in cells transfected with TLR2 and TLR5, but not TLR4. Consistent with the HEK293 experiments, H. pylori-induced NF-kappa B activation was decreased in MKN45 gastric epithelial cells by transfection of dominant-negative versions of TLR2 and TLR5 but not TLR4. Highly purified lipopolysaccharide from H. pylori strain 26695 activated NF-kappa B in HEK293 via TLR2 but not TLR4. Partially purified flagellin from H. pylori was also capable of inducing NF-kappa B activation in HEK cells transfected with TLR5. Additionally, chemokine gene expression was induced by H. pylori in HEK293 cells following stable transfection with TLR2 or TLR5 expression plasmids. These studies demonstrate that gastric epithelial cells recognize and respond to H. pylori infection at least in part via TLR2 and TLR5. Furthermore, the unique lipopolysaccharide of H. pylori is a TLR2, not a TLR4 agonist.

1951 related Products with: Toll-like receptor (TLR) 2 and TLR5, but not TLR4, are required for Helicobacter pylori-induced NF-kappa B activation and chemokine expression by epithelial cells.

3-O-Acetyl-17-O-tert-buty Androgen Receptor Ab 1 Androgen Receptor Antibod Androgen Receptor Ab-1 An Androgen Receptor 17β-Acetoxy-2α-bromo-5 4-Amino-1-tert-butyl-3-(1 Bradykinin receptor B1 An Rabbit Anti-kappa Opioid Androgen Receptor (Ab 650 Rabbit anti Androgen Rece Recombinant Human Androge

Related Pathways