Search results for: EnzyChrom™ Kinase Assay Kit
#29344656 // Save this To Up
Liraglutide suppresses proliferation and induces adipogenic differentiation of 3T3-L1 cells via the Hippo-YAP signaling pathway.Liraglutide, as a glucagon-like peptide‑1 analogue, is used to treat type 2 diabetes mellitus and obesity. Previous findings have demonstrated the effects of liraglutide on adipogenesis; however, the underlying mechanism involved in this process remains to be elucidated. In the present study, to certify the effect of liraglutide on adipogenesis and explore the possible underlying mechanism involved in this process, preadipocyte 3T3‑L1 cells were cultured in adipocyte‑inducing medium and treated with liraglutide. Subsequently, the expression levels of the master transcription factors and adipocyte‑specific genes were measured by reverse transcription‑quantitative polymerase chain reaction and immunoblotting analysis. Lipid droplet production was detected by Oil red O staining. Cell proliferation was determined by a Cell Counting Kit-8 assay and cell immunofluorescence for Ki67, and apoptosis was assessed by flow cytometry. Next, the expression levels of the core components in the Hippo‑yes‑associated protein (YAP) signaling pathway as well as YAP‑specific target genes were measured. Finally, short interfering RNAs of mammalian ste20 kinase 1/2 (MST1/2), a key protein kinase in the Hippo‑YAP pathway, were used to determine whether liraglutide regulated adipogenic differentiation via the Hippo‑YAP pathway. It was demonstrated that liraglutide promoted adipogenic differentiation, suppressed proliferation, did not affect apoptosis of 3T3‑L1 cells and activated the Hippo‑YAP signaling pathway at the initial stage of adipogenesis. Silencing of MST1 counteracted the effect of increasing adipogenesis by liraglutide. These results suggested that liraglutide may activate the Hippo‑YAP signaling pathway leading to the inhibition of proliferation of preadipocyte 3T3‑L1 cells, and result in cells achieving transformation into mature adipocytes sooner. Taken together, the results of the present study may expand knowledge of the underlying mechanism of liraglutide facilitating adipogenesis, and may contribute to the development of GLP‑1 receptor agonists for weight loss and increased insulin sensitivity.
2028 related Products with: Liraglutide suppresses proliferation and induces adipogenic differentiation of 3T3-L1 cells via the Hippo-YAP signaling pathway.Epidermal Growth Factor ( Epidermal Growth Factor ( AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF Hh Signaling Pathway Anta Rat Mesenchymal Cells Mesenchymal Stem Cell Adi anti CD7 All T cells Reco anti Transferrin receptor SRE Reporter - HEK293 Cel JAK pathway ISRE reporter Nrf antioxidant pathway A
#29343273 // Save this To Up
INPP4B promotes cell survival via SGK3 activation in NPM1-mutated leukemia.Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1) has been recognized as a distinct leukemia entity in the 2016 World Health Organization (WHO) classification. The genetic events underlying oncogenesis in NPM1-mutated AML that is characterized by a normal karyotype remain unclear. Inositol polyphosphate 4-phosphatase type II (INPP4B), a new factor in the phosphoinositide-3 kinase (PI3K) pathway-associated cancers, has been recently found a clinically relevant role in AML. However, little is known about the specific mechanistic function of INPP4B in NPM1-mutated AML.
2267 related Products with: INPP4B promotes cell survival via SGK3 activation in NPM1-mutated leukemia.Hairy Cell Leukemia; Clo Hairy Cell Leukemia; Clo Hairy Cell Leukemia; Clo anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl CELLKINES Natural Human I CELLKINES INTERLEUKIN 2 ( CELLKINES INTERLEUKIN 2 ( Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu
#29340041 // Save this To Up
Discovery of a highly selective KIT kinase primary V559D mutant inhibitor for gastrointestinal stromal tumors (GISTs).KIT kinase V559D mutation is the most prevalent primary gain-of-function mutation in Gastrointestinal Stromal Tumors (GISTs). Here we reported a highly selective KIT V559D inhibitor CHMFL-KIT-031, which displayed about 10-20 fold selectivity over KIT wt in the biochemical assay (IC50: 28 nM over 168 nM; Kd: 266 nM versus 6640 nM) and in cell (EC50: 176 nM versus 2000 nM for pY703) examination. It also displayed 15∼400-fold selectivity over other primary mutants such as L576P and secondary mutants including T670I, V654A (ATP binding pocket) as well as N822K and D816V (activation loop). In addition, it exhibited a selectivity S score (1) of 0.01 among 468 kinases/mutants in the KINOMEScan™ assay. CHMFL-KIT-031 showed potent inhibitory efficacy for KIT V559D mediated signaling pathways in cell and anti-tumor activity in vivo (Tumor Growth Inhibition: 68.5%). Its superior selectivity would make it a good pharmacological tool for further dissection of KIT V559D mediated pathology in the GISTs.
1557 related Products with: Discovery of a highly selective KIT kinase primary V559D mutant inhibitor for gastrointestinal stromal tumors (GISTs).EnzyChrom™ Kinase Assay Amplite™ Fluorimetric F Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor ATM Kinase Inhibitor ATM Kinase Inhibitor, KU- ATM Kinase Inhibitor, KU- Akt Inhibitor, Isozyme Se Primary antibody Caspase Primary antibody FLIP An
#29338725 // Save this To Up
Herbal formula YGJDSJ inhibits anchorage-independent growth and induces anoikis in hepatocellular carcinoma Bel-7402 cells.Based on clinical medications and related studies, we established a Yang-Gan Jie-Du Sang-Jie (YGJDSJ) herbal formula for hepatocarcinoma treatment. In present study, we evaluated the anti-cancer potential of YGJDSJ on suspension-grown human hepatocellular carcinoma Bel-7402 cells.
1705 related Products with: Herbal formula YGJDSJ inhibits anchorage-independent growth and induces anoikis in hepatocellular carcinoma Bel-7402 cells.Liver hepatocellular carc Liver cancer (hepatocellu Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Normal liver and hepatoce anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor (
#29330760 // Save this To Up
Oxidized phospholipids stimulate production of stem cell factor via NRF2-dependent mechanisms.Receptor tyrosine kinase c-Kit and its ligand stem cell factor (SCF) regulate resident vascular wall cells and recruit circulating progenitors. We tested whether SCF may be induced by oxidized palmitoyl-arachidonoyl-phosphatidylcholine (OxPAPC) known to accumulate in atherosclerotic vessels. Gene expression analysis demonstrated OxPAPC-induced upregulation of SCF mRNA and protein in different types of endothelial cells (ECs). Elevated levels of SCF mRNA were observed in aortas of ApoE-/- knockout mice. ECs produced biologically active SCF because conditioned medium from OxPAPC-treated cells stimulated activation (phosphorylation) of c-Kit in naïve ECs. Induction of SCF by OxPAPC was inhibited by knocking down transcription factor NRF2. Inhibition or stimulation of NRF2 by pharmacological or molecular tools induced corresponding changes in SCF expression. Finally, we observed decreased levels of SCF mRNA in aortas of NRF2 knockout mice. We characterize OxPLs as a novel pathology-associated stimulus inducing expression of SCF in endothelial cells. Furthermore, our data point to transcription factor NRF2 as a major mediator of OxPL-induced upregulation of SCF. This mechanism may represent one of the facets of pleiotropic action of NRF2 in vascular wall.
2703 related Products with: Oxidized phospholipids stimulate production of stem cell factor via NRF2-dependent mechanisms.Human Stem Cell Factor SC Macrophage Colony Stimula Macrophage Colony Stimula Mouse Stem Cell Factor SC Rat Stem Cell Factor SCF 129 Mouse Embryonic Stem Rat Mesenchymal Stem Cell ELISA Human , Stem Cell F Epidermal Growth Factor ( Epidermal Growth Factor ( TCGF (Natural T Cell Grow CELLKINES MACROPHAGE COLO
#29330663 // Save this To Up
Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction.Human cytomegalovirus (HCMV) infection has been linked to the pathogenesis of vasculopathy by inducing dysfunction of vascular cells such as endothelial cells. Hcmv-miR-UL112 is the most well-characterized HCMV-encoded microRNA occurring in the plasma of patients with cardiovascular diseases such as hypertension, while the specific underlying pathophysiological mechanisms are yet to be defined. The current study investigated the effect of hcmv-miR-UL112 on the growth and proliferation of human umbilical vascular endothelial cells (HUVECs); it might also be associated with signaling pathways. An adenovirus vector was designed and synthesized to stably express hcmv-miR-UL112 in HUVECs. Cell Counting Kit-8 results showed that ectopically expressed hcmv-miR-UL112 can significantly increase the proliferation of HUVECs (p < 0.05). Flow cytometry revealed that the S-phase fraction in the cell cycle analysis was raised significantly after overexpression of hcmv-miR-UL112 (p < 0.05). Gene expression profile analysis, using the microarray technology, revealed 303 up-regulated and 62 down-regulated genes in HUVECs by comparing the AD-hcmv-miR-UL112-infected and control groups (p < 0.05 and > 2 fold change). Kyoto Encyclopedia of Genes and Genomes and Reactome Pathway, chosen as the functional annotation categories, were affected by hcmv-miR-UL112 adenovirus vector. The significantly altered pathways mainly include the mitogen-activated protein kinase signaling pathway, cell adhesion molecules, chemokine signaling pathway, cytokine-cytokine receptor interaction, circadian rhythm-mammal, mineral absorption, protein processing in the endoplasmic reticulum, proximal tubule bicarbonate reclamation, vasopressin-regulated water reabsorption, and arachidonic acid metabolism. In conclusion, hcmv-miR-UL112 could serve as a potential biomarker, and the miRNA-mediated regulation of signaling pathways might play significant roles in the physiological effects of hcmv-associated diseases.
2338 related Products with: Human cytomegalovirus-encoded miR-UL112 contributes to HCMV-mediated vascular diseases by inducing vascular endothelial cell dysfunction.Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Human Tonsil Microvascula Human vascular cell adhes Mouse Vascular Endothelia Human soluble vascular ce Recombinant Human Vascula Mouse Vascular Endothelia Mouse Vascular Endothelia Rat Vascular Endothelial Rabbit Anti-Cell death in
#29328385 // Save this To Up
Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis.
2944 related Products with: Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.AKT PKB Signaling Phospho Human Epstein-Barr Virus Hh Signaling Pathway Anta Mouse Epstein-Barr Virus AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF BYL-719 Mechanisms: PI3K- Apoptosis antibody array AKT Phospho-Specific Arra AMPK Signaling Phospho-Sp Cancer Apoptosis Phospho- ErbB Her Signaling Phosph
#29312652 // Save this To Up
Tyrosine kinase inhibitor sensitive PDGFRΑ mutations in GIST: Two cases and review of the literature.Gastrointestinal stromal tumors (GISTs) are rare mesenchymal malignancies of the gastrointestinal tract. Most GISTs harbor a c-KIT (80%) or a PDGFRα (10%) mutation that leads to constitutive activation of the tyrosine kinase receptor. Response to treatment with tyrosine kinase inhibitors (TKIs) is dependent on mutational status of the tumor. The most common mutation in PDGFRα, D842V, is known to be imatinib resistant. Almost all other PDGFRα mutations are imatinib sensitive. We describe two patients with a PDGFRα exon 18 mutated GIST responding to treatment with TKIs. One of these patients has a p.M844_S847 deletion, not previously described in relation with TKI treatment response. Mutations in circulating tumor DNA were detectable with digital droplet PCR in serial plasma samples taken during treatment and correlated with treatment response of both patients. Computer 3D-modeling of the PDGFRα kinase domain of these two variants revealed no direct interference in imatinib or sunitinib binding and no effect in its activity in contrast to the reported structure of the imatinib resistant D842V mutation. An overview is given of the literature regarding the evidence of patients with different PDGFRα mutated GISTs on response to TKIs. The findings emphasize the use of mutational analysis in GIST to provide patients personalized treatment. Detection of mutations in plasma is feasible and can provide real-time information concerning treatment response. We suggest to register GIST patients with these uncommon mutations in a prospective international database to understand the tumor biology and obtain more evidence of such mutations to predict treatment response.
2938 related Products with: Tyrosine kinase inhibitor sensitive PDGFRΑ mutations in GIST: Two cases and review of the literature.DiscoveryPak™ EGFR Tyro DiscoveryPak™ Receptor Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor Aurora Kinase B Inhibitor ATM Kinase Inhibitor ATM Kinase Inhibitor, KU- ATM Kinase Inhibitor, KU- IKK-ε Kinase Inhibitor I IKK-ε Kinase Inhibitor I BI-6727 Mechanisms: Polo-
#29308510 // Save this To Up
[SiRNA silencing Rsk2 gene expression inhibits proliferation and osteogenic differentiation of human periodontal ligament cells].To study the effect of ribosomal S6 kinase (Rsk2) gene on proliferation and osteogenic differentiation of human periodontal ligament cells (hPDLCs) and underlying mechanism.
2009 related Products with: [SiRNA silencing Rsk2 gene expression inhibits proliferation and osteogenic differentiation of human periodontal ligament cells].Epidermal Growth Factor ( Epidermal Growth Factor ( Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Anti C Reactive Protein A Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon Growth Differentiation Fa Growth Differentiation Fa DNA (cytosine 5) methyltr
#29306537 // Save this To Up
Metformin Enhances the Differentiation of Dental Pulp Cells into Odontoblasts by Activating AMPK Signaling.Metformin is a first-line drug for treating type 2 diabetes that regulates the differentiation of mesenchymal stem cells. Its effects on human dental pulp cells (DPCs) remain unknown. This study aimed to investigate the effects of metformin on the proliferation and differentiation of DPCs.
1868 related Products with: Metformin Enhances the Differentiation of Dental Pulp Cells into Odontoblasts by Activating AMPK Signaling.Epidermal Growth Factor ( Epidermal Growth Factor ( AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF AMPK Signaling Phospho-Sp Fontana-Masson Stain Kit Fontana-Masson Stain Kit AMPKâ„¢1 (dn) AMPKâ„¢2 (dn) AMPKâ„¢2 (constitutiv Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia