Search results for: Nuclear Protein _ Human Tumor Cell Line Raji
#28976731 // Save this To Up
Targeted Disruption of Myc-Max Oncoprotein Complex by a Small Molecule.Myc plays important roles in cell cycle progression, cell growth, and stem cell self-renewal. Although dysregulation of Myc expression is a hallmark of human cancers, there is no Myc targeted therapy yet. Here, we report sAJM589, a novel small molecule Myc inhibitor, identified from a PCA-based high-throughput screen. sAJM589 potently disrupts the Myc-Max heterodimer in a dose dependent manner with an ICof 1.8 ± 0.03 μM. sAJM589 preferentially inhibits transcription of Myc target genes in a Burkitt lymphoma cell model, P493-6. Genome-wide transcriptome analysis showed that sAJM589 treatment and Myc depletion induced similar gene expression profiles. Consistently, sAJM589 suppressed cellular proliferation in diverse Myc-dependent cancer cell lines and anchorage independent growth of Raji cells. Disruption of the Myc-Max interaction by sAJM589 reduced Myc protein levels, possibly by promoting ubiquitination and degradation of Myc. Collectively, these results suggest that sAJM589 may be a basis for the development of potential inhibitors of Myc-dependent cell growth.
Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Mouse monoclonal Anti c M Mouse monoclonal Anti c M Dengue antibody (Complex) APAAP Complex antibody, M Myc (Phospho Thr58) Antib Myc (Phospho Thr358) Anti Myc (Phospho Ser373) Anti Myc (Phospho Ser62) Antib
#28666825 // Save this To Up
Triptonide acts as a novel potent anti-lymphoma agent with low toxicity mainly through inhibition of proto-oncogene Lyn transcription and suppression of Lyn signal pathway.Lyn is a proto-oncogene overexpressed and constitutively activated in lymphoma, and plays an important role in lymphoma initiation and malignant progression. Hence, the oncogenic Lyn has recently been targeted for novel anti-lymphoma drug discovery; however, the effective Lyn-targeted drug for lymphoma treatment with low toxicity is absent in the clinical setting. The goal of this study is to explore powerful and low toxic Lyn-targeted anti-lymphoma agent. Here we show that triptonide, a small molecule purified from the herb Tripterygium wilfordii Hook F, potently inhibits the proliferation of human B-lymphoma Raji and T-lymphoma Jurkat cells with IC50 of 5.7nM and 4.8nM, respectively. Strikingly, triptonide at a dose of 5mg/kg/day almost completely inhibited the lymphoma growth in human lymphoma cells-xenografted mice without obvious side effects, particularly; the tumors in 6 mice among the 8 xenografted mice were completely eradicated in vivo. Cell biological studies showed that triptonide at the doses of 2.5-10nM notably suppressed B-lymphoma cell colony-forming capability, and that triptonide at the dose of 20nM promoted apoptosis through activation of PARP and caspase 3, but reduction of BCL2 protein levels in the lymphoma cells. Molecular studies revealed that triptonide markedly inhibited oncogenic Lyn transcription through suppressing the promoter activity of the gene, and that it remarkably reduced both total and phosphorylated Lyn proteins, and diminished Lyn downstream ERK and ATK signal pathways. Additionally, triptonide significantly enhanced p38 phosphorylation. Together, triptonide exerts potent anti-lymphoma effect with low toxicity mainly through inhibition of proto-oncogene Lyn transcription and suppression of Lyn downstream ERK and ATK signal pathways, providing an attractive drug candidate for development of novel anti-lymphoma therapeutics.
2019 related Products with: Triptonide acts as a novel potent anti-lymphoma agent with low toxicity mainly through inhibition of proto-oncogene Lyn transcription and suppression of Lyn signal pathway.Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona Rabbit Anti-Lyn Polyclona
#28651105 // Save this To Up
Heterogeneous epigenetic regulation of HACE1 in Burkitt- Lymphoma-derived cells.We examined the consequences of 3-deazaneplanocin A (DZNep) on HACE1 expression in human Burkitt- Lymphoma-derived cells to investigate fundamental molecular mechanisms that control its expression. We treated the human Burkitt- Lymphoma-derived cells lines Ramos and Raji with DZNep and examined HACE1 mRNA expression by RT-PCR. We also studied the effect of DZNep on the methylation of lysine 9 and 27 of histone 3 (H3K27me3 and H3K9me2) associated with the CpG88 and CpG177 islands of the HACE1 promoters by chromatin immunoprecipitation and quantitative PCR. CpG88 (hypomethylated) of the HACE1 promoter was enriched for histone marks H3K27me3 and H3K9me2 whereas CpG177 (hypermethylated) was only enriched for H3K9me2. DZNep treatment increased HACE1 gene expression which was further increased by the addition of trichostatine A (TSA), a promising therapeutic compound for the treatment of human B-Lymphoma. Histone methylation (both H3K9me2 and H3K27me3) of the HACE1 promoter concomitantly decreased. Our experiments suggest that HACE1 can be downregulated by methylation of its promoter region chromatin (H3K27me3 and H3K9me2), making HACE1 a potential target for DZNep combined with TSA. These results highlight the heterogeneity of HACE1 regulation in B-lymphoma and suggest that successful drug-induced restoration of epigenetically silenced tumor suppressor genes will require accurate characterization of cell type- and locus-specific gene silencing mechanisms.
2942 related Products with: Heterogeneous epigenetic regulation of HACE1 in Burkitt- Lymphoma-derived cells.DNA (cytosine 5) methyltr GLP 2 ELISA Kit, Rat Prog anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( Macrophage Colony Stimula Macrophage Colony Stimula GLP 1 ELISA Kit, Rat Gluc C Peptide ELISA Kit, Rat Glucagon ELISA KIT, Rat G
#28222771 // Save this To Up
Wogonin as a targeted therapeutic agent for EBV (+) lymphoma cells involved in LMP1/NF-κB/miR-155/PU.1 pathway.Wogonin is an encouraging choice for clinical use owing to its potent anti-tumor and anti-inflammatory effects with the high safety profile. However, wogonin for targeted therapy of lymphoma was not well addressed. In this study, we focused on its anticancer effect alongside with the underlying mechanisms for targeted therapy in EBV-positive lymphoma. This will facilitate its introduction to clinical use, which is planned in the near future.
2480 related Products with: Wogonin as a targeted therapeutic agent for EBV (+) lymphoma cells involved in LMP1/NF-κB/miR-155/PU.1 pathway.Cancer Apoptosis Phospho- anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl EMAP II Inhibitor Z ASTD EMAP II Inhibitor Z ASTD Goat Anti-Human PU.1, (in GLP 1 ELISA Kit, Rat Gluc MMP-13 inhibitor assay ki CometAssay Control Cells Neutral CometAssay Contro AP-1 Reporter – HEK293 ASP-3026 Mechanisms: ALK
#28084852 // Save this To Up
Effects of digoxin on cell cycle, apoptosis and NF-κB pathway in Burkitt's lymphoma cells and animal model.Digoxin has potential antitumor properties. This study investigated whether digoxin suppressed Burkitt's lymphoma (BL) cells. Raji and NAMALWA cells were exposed to digoxin, followed by assay of cell viability, apoptosis and cell cycle. Western blotting was used to analyze NF-κB activity. A xenograft model was established for therapeutic efficacy evaluation. Digoxin inhibited cell growth and resulted in apoptosis and cell cycle arrest (G0/G1 for Raji cells; G2/M for NAMALWA cells). Digoxin inhibited DNA synthesis and induced morphological apoptotic characteristics. Besides, digoxin inhibited NF-κB and TNF-α-stimulated NF-κB activity, and suppressed NF-κB initiating genes (Bcl-2, Bcl-xL, cyclin D1, and c-myc), however, increased p21. Digoxin activated caspase-9/3. Furthermore, digoxin inhibited xenograft tumors growth and reduced Ki-67 and c-myc. Digoxin exerted antitumor effects on BL cells in vitro and in vivo might through regulating NF-κB and caspase pathway. These outcomes highlight the potential of digoxin as a therapeutic agent for BL.
2052 related Products with: Effects of digoxin on cell cycle, apoptosis and NF-κB pathway in Burkitt's lymphoma cells and animal model.Cell cycle antibody array Cell Cycle Phospho-Specif Macrophage Colony Stimula Macrophage Colony Stimula GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi Sf9 insect cells Sf21 insect cells superSf9-1 insect cells superSf9-2 insect cells
#27911272 // Save this To Up
FOXO4 expression is related to stem cell-like properties and resistance to treatment in diffuse large B-cell lymphoma.Cancer stem cells are proposed to be responsible for resistance to chemotherapeutic agents, including doxorubicin. As phenylbutyrate enhances cancer stem cell properties, we analyzed surviving lymphoma cells after treatment with doxorubicin and phenylbutyrate. Human B-cell lymphoma cell lines, including Toledo, BJAB, Daudi, and Raji were incubated with IC90 concentrations of doxorubicin (300 nM) or phenylbutyrate (8 mM). After 48 h, live cells were sorted and analyzed for their resistance to treatment by examining gene expression profiles using cDNA microarray and biological characteristics. A small fraction of lymphoma cells that survived after drug application showed higher expression of stem cell markers (NANOG, and SOX2) and superior ability of self-renewal and sphere formation, compared to untreated control cells (P < 0.05). Gene expression analysis disclosed elevated expression of 41 genes, including FOXO4, in the four lymphoma cell lines that survived drug treatment. Overexpression of FOXO4 was evident in lymphoma cells surviving after phenylbutyrate treatment and refractory patient-derived lymphoma cells. Induction of FOXO4 expression promoted self-renewal whereas its knockdown led to diminished expression of stem cell markers and colony-forming ability of lymphoma cells. Immunohistochemical staining for FOXO4 in tumor tissue of diffuse large B-cell lymphoma revealed nuclear localization and significant association with poor prognosis. In conclusion, lymphoma cells resistant to treatment exhibit stem cell-like properties and enhanced FOXO4 expression. The presence of FOXO4-expressing cells in tumor tissue and their association with poor survival supports a role of FOXO4 in promoting stem cell properties resulting in poor outcomes.
2179 related Products with: FOXO4 expression is related to stem cell-like properties and resistance to treatment in diffuse large B-cell lymphoma.Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Nycodenz, non ionic, non Diffuse large B cell lymp Diffuse large-B cell lymp Diffuse large B cell lymp Diffuse large B-cell lymp Oral squamous cell cancer Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in
#27720993 // Save this To Up
The interaction of protamine nanocapsules with the intestinal epithelium: A mechanistic approach.Single-layer protamine and double layer polysialic acid (PSA)/protamine nanocapsules (NCs) were designed in order to be used as carriers to facilitate the transport of macromolecules across the intestinal epithelium. The rational for the design of these NCs was based on that protamine is a non-toxic yet potent cell-penetrating peptide, capable of translocating protein cargos through cell membranes, while PSA is a low molecular weight polysaccharide used to enhance the stability of macromolecules and nanocarriers. The aim of this work was to study in vitro the mechanism of interaction of these NCs with different intestinal cell models (Caco-2, Caco-2/Raji mimicking follicle associated epithelium and Caco-2/HT29-MTX to study the effect of mucus). For this, a fluorescent marker, TAMRA was covalently linked to protamine. The interaction and transport of the NCs with the Caco-2 cells was found to be concentration, temperature and size dependent. In all cases, the double layer PSA-protamine NCs exhibited a significantly higher transport compared to protamine NCs. On the other hand, the transport of the NCs was significantly higher in the co-culture (Caco-2/Raji monolayer) compared to the monoculture model (Caco-2 monolayer), implying that M cells are involved in the transport of these nanosystems. The formulations, administered intra-jejunally to healthy rats (4h fasting) resulted in a moderate reduction of the glucose levels (20% reduction), which lasted for up to 4h. This work raises prospects that protamine-based nanocapsules may have the potential as oral peptide delivery nanocarriers.
1494 related Products with: The interaction of protamine nanocapsules with the intestinal epithelium: A mechanistic approach.TCP-1 theta antibody Sour Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Thermal Shaker with cooli Rat Anti-CCT theta Antibo Rabbit Anti-Theophylline Sheep Anti-Theophylline 3 FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu
#27796613 // Save this To Up
Catfish rhamnose-binding lectin induces Gcell cycle arrest in Burkitt's lymphoma cells via membrane surface Gb3.Silurus asotus egg lectin (SAL), an α-galactoside-binding protein isolated from the eggs of catfish, is a member of the rhamnose-binding lectin family that binds to Gb3 glycan (Galα1-4Galβ1-4Glc). We have previously demonstrated that SAL reduces the proliferation of Gb3-expressing Burkitt's lymphoma Raji cells and confirm here that it does not reduce their viability, indicating that unlike other lectins, it is not cytotoxic. The aim of this study was to determine the signal transduction mechanism(s) underlying this novel SAL/Gb3 binding-mediated effect profile. SAL/Gb3 interaction arrested the cell cycle through increasing the Gphase population of Raji cells. SAL suppressed the transcription of cell cycle-related factors such as c-MYC, cyclin D3, and cyclin-dependent protein kinase (CDK)-4. Conversely, the CDK inhibitors p21 and p27 were elevated by treatment with SAL. In particular, the production of p27 in response to SAL treatment increased steadily, whereas p21 production was maximal at 12 h and lower at 24 h. Activation of Ras-MEK-ERK pathway led to an increase in expression of p21. Notably, treatment of Raji cells with anti-Gb3 mAb alone did not produce the above effects. Taken together, our findings suggest that Gb3 on the Raji cell surface interacts with SAL to trigger sequential GDP-Ras phosphorylation, Ras-MEK-ERK pathway activation, p21 production, and cell cycle arrest at the Gphase.
2674 related Products with: Catfish rhamnose-binding lectin induces Gcell cycle arrest in Burkitt's lymphoma cells via membrane surface Gb3.Octyl â D 1 thioglucopyr Macrophage Colony Stimula Macrophage Colony Stimula Standard Pipet Tips200ul GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi Sf9 insect cells Sf21 insect cells superSf9-1 insect cells superSf9-2 insect cells
#27439606 // Save this To Up
Histone H4 is cleaved by granzyme A during staurosporine-induced cell death in B-lymphoid Raji cells.Granzyme A (GzmA) was first identified as a cytotoxic T lymphocyte protease protein with limited tissue expression. A number of cellular proteins are known to be cleaved by GzmA, and its function is to induce apoptosis. Histones H1, H2B, and H3 were identified as GzmA substrates during apoptotic cell death. Here, we demonstrated that histone H4 was cleaved by GzmA during staurosporine-induced cell death; however, in the presence of caspase inhibitors, staurosporine-treated Raji cells underwent necroptosis instead of apoptosis. Furthermore, histone H4 cleavage was blocked by the GzmA inhibitor nafamostat mesylate and by GzmA knockdown using siRNA. These results suggest that histone H4 is a novel substrate for GzmA in staurosporine-induced cells. [BMB Reports 2016; 49(10): 560-565].
2167 related Products with: Histone H4 is cleaved by granzyme A during staurosporine-induced cell death in B-lymphoid Raji cells.Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in
#27569089 // Save this To Up
Anticancer activity of Honokiol against lymphoid malignant cells via activation of ROS-JNK and attenuation of Nrf2 and NF-κB.To evaluate the effect of Honokiol (HK) in the ROS-JNK pro-apoptotic pathway and NF-κB, Nrf2 anti-apoptotic pathways, in order to seek a possible explanation for its anticancer efficacy.
2678 related Products with: Anticancer activity of Honokiol against lymphoid malignant cells via activation of ROS-JNK and attenuation of Nrf2 and NF-κB.MarkerGeneTM Live Cell Fl Ofloxacin CAS Number [824 Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri Rat Mesenchymal Cells anti CD7 All T cells Reco anti Transferrin receptor
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