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           Search results for: Mouse Anti Human CD34 CD34   

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Systemic multilineage engraftment in mice after in utero transplantation with human hematopoietic stem cells.

IUHCT of human cord blood-derived CD34+ cells into fetal NSG mice results in systemic multilineage engraftment with human cells.Preconditioning with in utero injection of an anti-c-Kit receptor antibody (ACK2) results in an improved rate of engraftment.

2310 related Products with: Systemic multilineage engraftment in mice after in utero transplantation with human hematopoietic stem cells.

Macrophage Colony Stimula Macrophage Colony Stimula Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl

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Modeling Anti-HIV-1 HSPC-Based Gene Therapy in Humanized Mice Previously Infected with HIV-1.

Investigations of anti-HIV-1 human hematopoietic stem/progenitor cell (HSPC)-based gene therapy have been performed by HIV-1 challenge after the engraftment of gene-modified HSPCs in humanized mouse models. However, the clinical application of gene therapy is to treat HIV-1-infected patients. Here, we developed a new method to investigate an anti-HIV-1 HSPC-based gene therapy in humanized mice previously infected with HIV-1. First, humanized mice were infected with HIV-1. When plasma viremia reached >107 copies/mL 3 weeks after HIV-1 infection, the mice were myeloablated with busulfan and transplanted with anti-HIV-1 gene-modified CD34+ HSPCs transduced with a lentiviral vector expressing two short hairpin RNAs (shRNAs) against CCR5 and HIV-1 long terminal repeat (LTR), along with human thymus tissue under the kidney capsule. Anti-HIV-1 vector-modified human CD34+ HSPCs successfully repopulated peripheral blood and lymphoid tissues in HIV-1 previously infected humanized mice. Anti-HIV-1 shRNA vector-modified CD4+ T lymphocytes showed selective advantage in HIV-1 previously infected humanized mice. This new method will be useful for investigations of anti-HIV-1 gene therapy when testing in a more clinically relevant experimental setting.

1501 related Products with: Modeling Anti-HIV-1 HSPC-Based Gene Therapy in Humanized Mice Previously Infected with HIV-1.

anti HIV 2 gp36 IgG1 (mon anti HIV 1 p55 17 IgG1 (m anti HIV 1 p17 IgG1 (mono anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Anti HIV 1 p24 Clone 38 8 MONOBODIES (Monoclonal An Anti-HIV-1 p17 Clone 32 5 Anti HIV 1 p17 Clone 32 5 MONOBODIES (Monoclonal An Anti-HIV-1 gp41 Clone 10E Anti HIV 1 gp41 Clone 10E

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Adipose tissue-derived stem cells in a fibrin implant enhance neovascularization in a peritoneal grafting site: a potential way to improve ovarian tissue transplantation.

Do two different concentrations of human adipose tissue-derived stem cells (ASCs) embedded inside a fibrin scaffold have the potential to differentiate into vessels and aid vascularization in a peritoneal grafting site intended for ovarian tissue transplantation?

1180 related Products with: Adipose tissue-derived stem cells in a fibrin implant enhance neovascularization in a peritoneal grafting site: a potential way to improve ovarian tissue transplantation.

Top five cancer tissue ar Ovarian cancer tissue arr FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Oral squamous cell cancer Ovarian cancer tissue arr Ovarian cancer tissue arr Ovarian disease spectrum Ovary disease spectrum (o Late stage ovarian tumor

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Transdifferentiation of human MNNG/HOS osteosarcoma cells into vascular endothelial cells in vitro and in vivo.

The transdifferentiation of cancer cells into other types of cells in several types of tissues or organs has been studied. However, whether human osteosarcoma MNNG/HOS cells can transdifferentiate into other types of cells has seldom been reported. Meanwhile, the mechanism of tumor angiogenesis is still disputed, and whether MNNG/HOS cells participate in angiogenesis in osteosarcoma remains unknown. In the present study, the investigation was divided into two parts: in vitro and in vivo. In vitro, we cultivated MNNG/HOS cells under hypoxic conditions for 4 days and found that they typically showed a characteristic 'flagstone' appearance as cultured vascular endothelial cells (VECs). MNNG/HOS cells that were cultivated on Matrigel under hypoxic conditions gradually formed tubular-like structures. Furthermore, when cultured under hypoxic conditions for 4 days, MNNG/HOS cells also transcribed and expressed several molecular markers of VECs (CD31, CD34 and vWF). In vivo, MNNG/HOS cells (1x106 cells) were cultivated under hypoxic conditions and subcutaneously injected into nude mice; the mice were sacrificed 49 days after inoculation. Immunohistochemical staining with anti-human CD31 antibody showed evidence of tumor angiogenesis in human osteosarcoma MNNG/HOS cells. The results demonstrated that MNNG/HOS cells can transdifferentiate into vascular endothelial cell-like cells in vitro and in vivo.

1399 related Products with: Transdifferentiation of human MNNG/HOS osteosarcoma cells into vascular endothelial cells in vitro and in vivo.

Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Macrophage Colony Stimula Macrophage Colony Stimula MarkerGeneTM in vivo lacZ anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Goat Anti-Human Endotheli GLP 1 ELISA Kit, Rat Gluc

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Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo.

Ginsenoside Rk3 (Rk3) is present in the roots of processed Panax notoginseng herbs and it exerts anti-platelet aggregation, pro-immunogenic and cardioprotective effects. However, little is known regarding the anticancer activities of this compound, especially in lung cancer. This study was designed to investigate the anticancer effects of Rk3 on non-small cell lung cancer (NSCLC) cells and in an H460 xenograft tumor model. Our results showed that Rk3 reduced cell viability, inhibited both cell proliferation and colony formation, and induced G1 phase cell cycle arrest by downregulating the expression of cyclin D1 and CDK4 and upregulating the expression of P21. Rk3 also induced apoptosis in a concentration-dependent manner in H460 and A549 cells by Annexin V/PI staining, TUNEL assay and JC-1 staining, resulting in a change in the nuclear morphology. Moreover, Rk3 induced the activation of caspase-8, -9, and -3, promoted changes in mitochondrial membrane potential, decreased the expression of Bcl-2, increased the expression of Bax, and caused the release of cytochrome c, which indicated that the apoptosis-inducing effects of Rk3 were triggered via death receptor-mediated mitochondria-dependent pathways. Furthermore, Rk3 significantly inhibited the growth of H460 xenograft tumors without an obvious effect on the body weight of the treated mice. Histological analysis indicated that Rk3 inhibited tumor growth by altering the proliferation and morphology of tumor cells. In addition, we confirmed that Rk3 inhibited angiogenesis via CD34 staining and chick embryo chorioallantoic membrane (CAM) assay in vivo. Taken together, our findings revealed not only the anticancer effect of Rk3 on NSCLC cells but also a new promising therapeutic agent for human NSCLC.

1721 related Products with: Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo.

Lung non small cell cance Non-small cell lung cance Human Small Intestine Mic Small cell lung carcinoma Non small cell lung carci Non small cell lung carci Lung small cell carcinoma High density non small ce Middle advanced stage lun Multiple lung carcinoma ( MarkerGeneTM in vivo lacZ anti HSV (II) gB IgG1 (mo

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A water-soluble polysaccharide from the roots of Polygala tenuifolia suppresses ovarian tumor growth and angiogenesis in vivo.

PTP, one polysaccharide extracted from the roots of Polygala tenuifolia, has displayed anti-cancer activity in several types of ovarian cancer cells. This study aims to elucidate the structure of PTP and investigate its anticancer effects against SKOV3 xenograft tumor growth in BALB/c mice, as well as the underlying mechanisms involved. GC-MS and NMR data indicate that PTP has a backbone composed of 1,4,6-linked-β-Galp, 1,4-linked-β-Galp and 1,4-linked-β-Glcp, with non-reducing terminal 1-linked-α-Glcp attached to O-6 of 1,4,6-linked-β-Galp. The tumor growth was suppressed in mice following two week's PTP administration (10, 20 and 40mg/kg) due to the induction of apoptosis, as detected by TUNEL assay. Moreover, lower serum VEGF and EGFR levels were observed in BALB/c mice treated with different doses of PTP when compared with that in untreated mice. Also, EGFR, VEGF, and CD34 were decreased in both transcript and protein levels in the tumor-bearing mice upon PTP treatment. Taken together, our data suggest that PTP appears to be a powerful chemopreventive agent for the patients with ovarian cancer, especially at advanced stage.

2087 related Products with: A water-soluble polysaccharide from the roots of Polygala tenuifolia suppresses ovarian tumor growth and angiogenesis in vivo.

Directed In Vivo Angiogen Multiple organ tumor tiss Late stage ovarian tumor Tissue array of ovarian g RANK Ligand Soluble, Huma Cultrex In Vitro Angiogen IGF-1R Signaling Phospho- Angiogenesis (Human) Anti Angiogenesis (Human) Anti Angiogenesis (Mouse) Anti Angiogenesis (Human) Anti Angiogenesis (Human) Anti

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Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells.

Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or third-generation c-Abl-specific tyrosine kinase inhibitors (TKIs) has substantially extended patient survival. However, TKIs primarily target differentiated cells and do not eliminate leukemic stem cells (LSCs). Therefore, targeting minimal residual disease to prevent acquired resistance and/or disease relapse requires identification of new LSC-selective target(s) that can be exploited therapeutically. Considering that malignant transformation involves cellular metabolic changes, which may in turn render the transformed cells susceptible to specific assaults in a selective manner, we searched for such vulnerabilities in CML LSCs. We performed metabolic analyses on both stem cell-enriched (CD34+ and CD34+CD38-) and differentiated (CD34-) cells derived from individuals with CML, and we compared the signature of these cells with that of their normal counterparts. Through combination of stable isotope-assisted metabolomics with functional assays, we demonstrate that primitive CML cells rely on upregulated oxidative metabolism for their survival. We also show that combination treatment with imatinib and tigecycline, an antibiotic that inhibits mitochondrial protein translation, selectively eradicates CML LSCs both in vitro and in a xenotransplantation model of human CML. Our findings provide a strong rationale for investigation of the use of TKIs in combination with tigecycline to treat patients with CML with minimal residual disease.

1580 related Products with: Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells.

Macrophage Colony Stimula Macrophage Colony Stimula Stemez hN2 Human Neuron D Rat monoclonal anti mouse Rat monoclonal anti mouse 129 Mouse Embryonic Stem Rat Mesenchymal Stem Cell Hairy Cell Leukemia; Clo Hairy Cell Leukemia; Clo Hairy Cell Leukemia; Clo Fontana-Masson Stain Kit Fontana-Masson Stain Kit

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Ruxolitinib/nilotinib cotreatment inhibits leukemia-propagating cells in Philadelphia chromosome-positive ALL.

As one of the major treatment obstacles in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL), relapse of Ph+ALL may result from the persistence of leukemia-propagating cells (LPCs). Research using a xenograft mouse assay recently determined that LPCs were enriched in the CD34+CD38-CD58- fraction in human Ph+ALL. Additionally, a cohort study demonstrated that Ph+ALL patients with a LPCs phenotype at diagnosis exhibited a significantly higher cumulative incidence of relapse than those with the other cell phenotypes even with uniform front-line imatinib-based therapy pre- and post-allotransplant, thus highlighting the need for novel LPCs-based therapeutic strategies.

1538 related Products with: Ruxolitinib/nilotinib cotreatment inhibits leukemia-propagating cells in Philadelphia chromosome-positive ALL.

anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl DNA (cytosine 5) methyltr Macrophage Colony Stimula Macrophage Colony Stimula GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi Sf9 insect cells

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A new monoclonal antibody detects downregulation of protein tyrosine phosphatase receptor type γ in chronic myeloid leukemia patients.

Protein tyrosine phosphatase receptor gamma (PTPRG) is a ubiquitously expressed member of the protein tyrosine phosphatase family known to act as a tumor suppressor gene in many different neoplasms with mechanisms of inactivation including mutations and methylation of CpG islands in the promoter region. Although a critical role in human hematopoiesis and an oncosuppressor role in chronic myeloid leukemia (CML) have been reported, only one polyclonal antibody (named chPTPRG) has been described as capable of recognizing the native antigen of this phosphatase by flow cytometry. Protein biomarkers of CML have not yet found applications in the clinic, and in this study, we have analyzed a group of newly diagnosed CML patients before and after treatment. The aim of this work was to characterize and exploit a newly developed murine monoclonal antibody specific for the PTPRG extracellular domain (named TPγ B9-2) to better define PTPRG protein downregulation in CML patients.

1489 related Products with: A new monoclonal antibody detects downregulation of protein tyrosine phosphatase receptor type γ in chronic myeloid leukemia patients.

Interferon-a Receptor Typ Anti 3 DG imidazolone Mon Anti-Infectious Pancreati Anti-Infectious Pancreati Anti-Infectious Pancreati anti-Protein Tyrosine pho Polyclonal Antibody Recep Anti-BMPR1A(Bone morphoge Anti-BMPR1B(Bone morphoge Monoclonal Anti-Alkaline Anti C Reactive Protein A MOUSE ANTI BOVINE ROTAVIR

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EV-3, an endogenous human erythropoietin isoform with distinct functional relevance.

Generation of multiple mRNAs by alternative splicing is well known in the group of cytokines and has recently been reported for the human erythropoietin (EPO) gene. Here, we focus on the alternatively spliced EPO transcript characterized by deletion of exon 3 (hEPOΔ3). We show co-regulation of EPO and hEPOΔ3 in human diseased tissue. The expression of hEPOΔ3 in various human samples was low under normal conditions, and distinctly increased in pathological states. Concomitant up-regulation of hEPOΔ3 and EPO in response to hypoxic conditions was also observed in HepG2 cell cultures. Using LC-ESI-MS/MS, we provide first evidence for the existence of hEPOΔ3 derived protein EV-3 in human serum from healthy donors. Contrary to EPO, recombinant EV-3 did not promote early erythroid progenitors in cultures of human CD34+ haematopoietic stem cells. Repeated intraperitoneal administration of EV-3 in mice did not affect the haematocrit. Similar to EPO, EV-3 acted anti-apoptotic in rat hippocampal neurons exposed to oxygen-glucose deprivation. Employing the touch-screen paradigm of long-term visual discrimination learning, we obtained first in vivo evidence of beneficial effects of EV-3 on cognition. This is the first report on the presence of a naturally occurring EPO protein isoform in human serum sharing non-erythropoietic functions with EPO.

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Goat Anti-Human Laforin ( SEC13 protein isoform 1 a muscleblind-like 3 isofor interleukin 17 receptor C cell cycle progression 2 Amphiphysiniphysin isofor steroidogenic acute regul alanine-glyoxylate aminot voltage-dependent calcium meckelin isoform 1 antibo amyloid beta precursor pr V-ATPase 116 kDa isoform

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