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#28765892   2017/08/02 Save this To Up

Production of bFGF monoclonal antibody and its inhibition of metastasis in Lewis lung carcinoma.

Basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor 1 (FGFR1) are associated with drug resistance in lung cancer. In the present study, mouse monoclonal antibodies (mAb) against human bFGF, targeting the binding site of bFGF with FGFR1 were produced, and the antitumor activity and inhibition of metastasis was studied in Lewis lung carcinoma (LLC). A total of four hybridoma cell strains that stably secreted bFGF mAb were obtained. mAbE12 was selected as the most effective for use in the following studies, with a relative affinity constant of 5.66x108 l/mol. mAbE12 was demonstrated to inhibit cell proliferation and tumor growth in vitro and in vivo. Furthermore, mAbE12 blocked migration and metastasis of LLC cells in vitro and in vivo. This occurred due to a mAbE12‑induced upregulation of E‑cadherin expression through the protein kinase B‑glycogen synthase kinase 3 β‑Snail pathway. These results suggested that mAbE12 may be a potential antibody for the treatment of lung cancer.

1390 related Products with: Production of bFGF monoclonal antibody and its inhibition of metastasis in Lewis lung carcinoma.

Small cell lung carcinoma Non small cell lung carci Non small cell lung carci Lung small cell carcinoma Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon HIV1 integrase antibody, Anti 3 DG imidazolone Mon Lung carcinoma and normal Lung carcinoma and normal

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#28435909   2017/04/24 Save this To Up

Self-assembled particulate PsaA as vaccine against Streptococcus pneumoniae infection.

Streptococcus pneumoniae is a human pathogen responsible for the majority of childhood pneumonia and media otitis cases worldwide. The diversity of its capsular polysaccharides (CPS) results in more than 91 serotypes of which at least 23 are virulent. Various CPS conjugated to immunogenic carrier proteins are currently licensed and provide protection against the infection caused by the respective serotypes but not against new and emerging virulent serotypes. In this study, we considered the conserved protein antigen PsaA, the pneumococcal surface adhesin A, in order to overcome the limitations of CPS antigens. The PsaA was translationally fused to a polyhydroxybutyrate (PHB) synthase which mediated production of PsaA displayed on PHB inclusions in recombinant Escherichia coli. This suggested that the PsaA fusion to the PHB synthase did not interfere with PHB synthase activity and its ability to mediate formation of nano-sized inclusions composed of a PHB core surrounded by the PHB synthase fused to PsaA. Isolated PHB beads showed a negative surface charge. Transmission electron microscopy analysis suggested that the PsaA fusion to the PHB synthase reduced the size of PHB beads from about 500 nm to 100 nm. The integrity and antigenicity of the fusion protein attached to isolated PHB beads was confirmed by SDS-PAGE, tryptic peptide fingerprinting analysis using MALDI-TOF-MS/MS and immunoblotting using a monoclonal anti-PsaA antibody. Mice immunized with PsaA displaying PHB beads produced high and specific IgG levels dominated by IgG1 isotype. While IgG1 titer were similar between soluble and insoluble PsaA, the IgG2 titers were strongly increased upon vaccination with insoluble PsaA i.e. PsaA displayed on PHB beads. Particulate PsaA-PHB beads elicited IgG antibodies recognizing PsaA in whole cell lysates of seven different serotypes of S. pneumoniae. This study suggested that PHB beads are suitable carriers for PsaA in order to induce a significant and specific Th-2-type immune response.

1524 related Products with: Self-assembled particulate PsaA as vaccine against Streptococcus pneumoniae infection.

Cytosol/Particulate Separ Cytosol Particulate Separ Cytosol Particulate Separ Rapid Microplate Assay K Astra Blue Solution Astra Blue Solution ASK2 ASK1 KM (dn) OXI TEK (Oxidative Stress TBARS Assay Kit TBARS Assay Kit (160 test BACTERIOLOGY KLEBSIELLA P

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#26515557   2016/03/04 Save this To Up

Dimethylarginine dimethylaminohydrolase 2 promotes tumor angiogenesis in lung adenocarcinoma.

Although embryonal proteins have been used as tumor marker, most are not useful for detection of early malignancy. In the present study, we developed mouse monoclonal antibodies against fetal lung of miniature swine, and screened them to find an embryonal protein that is produced at the early stage of malignancy, focusing on lung adenocarcinoma. We found an antibody clone that specifically stained stroma of lung adenocarcinoma. LC-MS/MS identified the protein recognized by this clone as dimethylarginine dimethylaminohydrolase 2 (DDAH2), an enzyme known for antiatherosclerotic activity. DDAH2 was found to be expressed in fibroblasts of stroma of malignancies, with higher expression in minimally invasive adenocarcinoma (MIA) and invasive adenocarcinoma than in adenocarcinoma in situ (AIS). Moreover, tumors with high stromal expression of DDAH2 had a poorer prognosis than those without. In vitro analysis showed that DDAH2 increases expression of endothelial nitric oxide synthase (eNOS), inducing proliferation and capillary-like tube formation of vascular endothelial cells. In resected human tissues, eNOS also showed higher expression in invasive adenocarcinoma than in AIS and normal lung, similarly to DDAH2. Our data indicate that expression of DDAH2 is associated with invasiveness of lung adenocarcinoma via tumor angiogenesis. DDAH2 expression might be a prognostic factor in lung adenocarcinoma.

1892 related Products with: Dimethylarginine dimethylaminohydrolase 2 promotes tumor angiogenesis in lung adenocarcinoma.

Colon adenocarcinoma tiss Lung tumor survey tissue Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Lung cancer tissue array, Lung carcinoma and normal Lung adenocarcinoma and n Lung adenocarcinoma tissu

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#23953854   2013/09/10 Save this To Up

Lymphocyte-mediated macrophage apoptosis during IL-12 stimulation.

In contrast to the well known immunostimulatory roles of IL-12, little has been known about its immunosuppressive roles. In the present study, IL-12-activated lymphocyte-mediated macrophage apoptosis was investigated by employing murine lymphocyte/macrophage cocultures. IL-12-activated lymphocytes and their culture supernatants induced an inducible nitric oxide synthase (iNOS)-mediated nitric oxide (NO) synthesis in macrophages. The NO synthesis was markedly inhibited by blocking antibodies to IFN-γ and TNF-α, suggesting the key role of these lymphocyte cytokines in mediating the NO synthesis. The endogenously produced NO inhibited macrophage proliferation, and induced apoptosis in concordance with the accumulation of p53, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and DR5, and the activation of caspase-3, processes that were inhibited by N(G)-monomethyl-l-arginine, aminoguanidine (NO synthase inhibitors) and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (an NO scavenger). These results were further supported by the findings obtained from the experiments employing IFN-γ-knockout and iNOS-knockout mice. Our study demonstrated a novel, non-contact-dependent mechanism of macrophage suppression by IL-12-activated lymphocytes: induction of growth inhibition and apoptosis of macrophages due to endogenous NO synthesis induced by cytokines secreted from IL-12-activated lymphocytes.

2518 related Products with: Lymphocyte-mediated macrophage apoptosis during IL-12 stimulation.

IL-12Rbeta1 antibody Sour IL-12p40, human recombina IL 12p40, human recombina IL 12p40, human recombina IL 12p40 Antibody Rabbit Anti-Human Apoptos CRF Anti-Polyvalent HRP EconoTek Alk-Phos Anti-P EconoTek HRP Anti-Polyva Retrieval HRP Anti-Polyv SensiTek Alk-Phos Anti-M SensiTek Alk-Phos Anti-P

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#23382985   2013/02/05 Save this To Up

Mannosyl-recognizing receptors induce an M1-like phenotype in macrophages of susceptible mice but an M2-like phenotype in mice resistant to a fungal infection.

In addition to alpha1,3 glucan, mannan and mannan-linked proteins are expressed in the outer layer of Paracoccidioides brasiliensis yeasts. The recognition of mannosyl residues by multiple pathogen recognition receptors, such as the mannose receptor (MR), complement receptor 3 (CR3) and toll-like receptor 4 (TLR4) on macrophage membranes can influence macrophage activation and the mechanisms of innate immunity against fungal pathogens. The aim of this study was to clarify the role of these receptors in the interaction between P. brasiliensis and macrophages from resistant (A/J) and susceptible (B10.A) mice. Therefore, the phagocytic, fungicidal and secretory abilities of macrophages were evaluated in the presence of mannan and antibodies against MR, CR3 and TLR4. We verified that mannan increased and anti-MR antibody decreased the killing ability and nitric oxide production of macrophages. The specific blockade of MR, CR3 and TLR4 by monoclonal antibodies impaired fungal recognition and modulated the production of cytokines. Mannan or P. brasiliensis induced decreased expression of MR and TLR2 on A/J macrophages, whereas CR3, TLR4 and TLR2 were reduced on B10.A cells. Importantly, both mannan and P. brasiliensis induced the production of IL-12 by B10.A macrophages, whereas TGF-β, TNF-α and IL-6 were produced by A/J cells. In addition, B10.A macrophages exhibited a prevalent expression of inducible NO-synthase and SOCS3 (suppressor of cytokine signaling-3), indicating a pro-inflammatory, "M1-like" differentiation. In contrast, the elevated expression of arginase-1, found in inflammatory zone-1 (FIZZ1), YM1 (CHI313, chitinase-like lectin), and SOCS1, typical markers of alternatively activated macrophages, indicates a prevalent "M2-like" differentiation of A/J macrophages. In conclusion, our data reveal that several mannosyl-recognizing receptors coordinate the apparently paradoxical innate response to paracoccidioidomycosis, in which resistance is initially mediated by alternatively activated phagocytes and tolerance to fungal growth, whereas susceptibility is linked to classically activated macrophages and the efficient control of fungal growth.

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Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon TGF beta induced factor 2 Nuclear Membrane Receptor Goat anti Influenza A M1 Mouse Anti-Influenza B Ma Goat Anti-Human TOM1L1 SR FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu

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#23140181   2012/11/22 Save this To Up

Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines.

Leukemia, a heterogeneous clonal disorder of hematopoietic progenitor cells, presents a world-wide health problem, especially in childhood. F1F0 ATPase, an inner mitochondrial enzyme, is expressed on the plasma membrane of tumor cells, and its inhibition induces both anti-angiogenic and anti-tumorigenic activity.

1574 related Products with: Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines.

MarkerGeneTM in vivo lacZ Anti-ATPase, (Na(+) K(+)) Anti ATPase, (Na(+) K(+)) Alamar Blue™, REDOX ind Alamar Blue™, REDOX ind 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 Epidermal Growth Factor (

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#22327435   2012/02/13 Save this To Up

New developments in malaria diagnostics: monoclonal antibodies against Plasmodium dihydrofolate reductase-thymidylate synthase, heme detoxification protein and glutamate rich protein.

Currently available rapid diagnostic tests (RDTs) for malaria show large variation in sensitivity and specificity, and there are concerns about their stability under field conditions. To improve current RDTs, monoclonal antibodies (mAbs) for novel malaria antigens have been developed and screened for their possible use in new diagnostic tests. Three antigens, glutamate rich protein (GLURP), dihydrofolate reductase-thymidylate synthase (DHFR-TS) and heme detoxification protein (HDP), were selected based on literature searches. Recombinant antigens were produced and used to immunize mice. Antibody-producing cell lines were subsequently selected and the resulting antibodies were screened for specificity against Plasmodium falciparum and Plasmodium vivax. The most optimal antibody couples were selected based on antibody affinity (expressed as dissociation constants, KD) and detection limit of crude antigen extract from P. falciparum 3D7 culture. The highest affinity antibodies have KD values of 0.10 nM ± 0.014 (D5) and 0.068 ± 0.015 nM (D6) for DHFR-TS mAbs, 0.10 ± 0.022 nM (H16) and 0.21 ± 0.022 nM (H18) for HDP mAbs and 0.11 ± 0.028 nM (G23) and 0.33 ± 0.093 nM (G22) for GLURP mAbs. The newly developed antibodies performed at least as well as commercially available histidine rich protein antibodies (KD of 0.16 ± 0.13 nM for PTL3 and 1.0 ± 0.049 nM for C1-13), making them promising reagents for further test development.

1370 related Products with: New developments in malaria diagnostics: monoclonal antibodies against Plasmodium dihydrofolate reductase-thymidylate synthase, heme detoxification protein and glutamate rich protein.

Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Mouse Anti-Influenza B Ma Goat Anti-Influenza A Mat Rabbit Anti-Rat Androgen Goat Anti-Human, Mouse GC Goat Anti-Rat Myelin Prot Goat Anti-Human Prion Pro

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#20337043   2010/03/26 Save this To Up

[Preparation of monoclonal antibody against lung cancer and identification of its targeting antigen].

A mouse-anti-human monoclonal antibody was produced by using the membrane proteins of human lung carcinoma cell line A549 as the immunogen to generate monoclonal antibodies against lung carcinoma with the use of hybridoma techniques. McAb4E7 was prepared successfully. To identify its antigen, proteomic technologies such as two-dimenstional electrophoresis, western blotting and mass spectrometry were employed. The targeting antigen of McAb4E7 expressed positive in human lung cancer cell lines A549 and human hepatocarcinoma cell line HepG2, moreover, the expression of the antigen was stronger in A549 cells. Finally, we obtained one positive protein in A549 cell line that has strong affinity and specificity for McAb4E7, which was identified to be ATP synthase beta subunit. We identified ATP synthase beta subunit as the targeting antigen of lung carcinoma special monoclonal antibody McAb4E7.

2946 related Products with: [Preparation of monoclonal antibody against lung cancer and identification of its targeting antigen].

anti CD54 IgG2b k monoclo anti CD66e IgG1 monoclona MOUSE ANTI BORRELIA BURGD serologically defined col Rabbit Anti-GAGE7 Cancer Anti Human Macrophage Sur MOUSE ANTI HUMAN EPITHELI Abeta (1-40 42) | 4D8 | o Monoclonal Anti-Breast Ca Monoclonal Anti-Breast Ca Anti-actin associated ant Cancer Antigen 50 (CA 50)

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#19944071   2010/01/27 Save this To Up

GMab-1, a high-affinity anti-3'-isoLM1/3',6'-isoLD1 IgG monoclonal antibody, raised in lacto-series ganglioside-defective knockout mice.

The lacto-series gangliosides 3'-isoLM1 and 3',6'-isoLD1 have been identified as tumor-associated antigens whose formation is initiated by the Lc3-synthase. Until now, high-affinity IgG monoclonal antibodies (mAbs) against 3'-isoLM1 and 3',6'-isoLD1, which are highly expressed in gliomas, have not been developed, although mAbs against lacto-series gangliosides are powerful tools for functional studies. We previously produced the Lc3-synthase gene beta3Gn-T5 knockout mice. In this study, we immunized beta3Gn-T5 knockout mice with 3'-isoLM1/3',6'-isoLD1 and produced the anti-3'-isoLM1/3',6'-isoLD1 mAb GMab-1, of the IgG(3) subclass, which should be useful for functional analysis of lacto-series gangliosides and for antibody-based therapy of gliomas.

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Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (18-39) Rabbit Anti-ACTH (1-39) P Rabbit Anti-ACTH (1-39) P Rabbit Anti-ACTH (1-39) P Rabbit Anti-ACTH (1-39) P Rabbit Anti-ACTH (1-39) P Rabbit Anti-ACTH (1-39) P

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#19920185   2009/12/16 Save this To Up

Acyl-CoA synthetase VL3 knockdown inhibits human glioma cell proliferation and tumorigenicity.

The contribution of lipid metabolic pathways to malignancy is poorly understood. Expression of the fatty acyl-CoA synthetase ACSVL3 was found to be markedly elevated in clinical malignant glioma specimens but nearly undetectable in normal glia. ACSVL3 levels correlated with the malignant behavior of human glioma cell lines and glioma cells propagated as xenografts. ACSVL3 expression was induced by the activation of oncogenic receptor tyrosine kinases (RTK) c-Met and epidermal growth factor receptor. Inhibiting c-Met activation with neutralizing anti-hepatocyte growth factor monoclonal antibodies reduced ACSVL3 expression concurrent with tumor growth inhibition in vivo. ACSVL3 expression knockdown using RNA interference, which decreased long-chain fatty acid activation, inhibited anchorage-dependent and anchorage-independent glioma cell growth by approximately 70% and approximately 90%, respectively. ACSVL3-depleted cells were less tumorigenic than control cells, and subcutaneous xenografts grew approximately 60% slower than control tumors. Orthotopic xenografts produced by ACSVL3-depleted cells were 82% to 86% smaller than control xenografts. ACSVL3 knockdown disrupted Akt function as evidenced by RTK-induced transient decreases in total and phosphorylated Akt, as well as glycogen synthase kinase 3beta, via a caspase-dependent mechanism. Expressing constitutively active myr-Akt rescued cells from the anchorage-dependent and anchorage-independent growth inhibitory effects of ACSVL3 depletion. These studies show that ACSVL3 maintains oncogenic properties of malignant glioma cells via a mechanism that involves, in part, the regulation of Akt function.

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Epidermal Growth Factor ( Epidermal Growth Factor ( T-cell proliferation grad TCHI T cell proliferation TCHI T cell proliferation T-cell proliferation grad TCHII T cell proliferatio TCHII T cell proliferatio Acyl CoA Synthase Acyl CoA binding Protein Anti C Reactive Protein A anti SLAM anti CDw150 IgG

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