搜索结果: 'easysep'

Haniffa M et al. (FEB 2009) The Journal of experimental medicine 206 2 371--85

Differential rates of replacement of human dermal dendritic cells and macrophages during hematopoietic stem cell transplantation.

Animal models of hematopoietic stem cell transplantation have been used to analyze the turnover of bone marrow-derived cells and to demonstrate the critical role of recipient antigen-presenting cells (APC) in graft versus host disease (GVHD). In humans,the phenotype and lineage relationships of myeloid-derived tissue APC remain incompletely understood. It has also been proposed that the risk of acute GVHD,which extends over many months,is related to the protracted survival of certain recipient APC. Human dermis contains three principal subsets of CD45(+)HLA-DR(+) cells: CD1a(+)CD14(-) DC,CD1a(-)CD14(+) DC,and CD1a(-)CD14(+)FXIIIa(+) macrophages. In vitro,each subset has characteristic properties. After transplantation,both CD1a(+) and CD14(+) DC are rapidly depleted and replaced by donor cells,but recipient macrophages can be found in GVHD lesions and may persist for many months. Macrophages isolated from normal dermis secrete proinflammatory cytokines. Although they stimulate little proliferation of naive or memory CD4(+) T cells,macrophages induce cytokine expression in memory CD4(+) T cells and activation and proliferation of CD8(+) T cells. These observations suggest that dermal macrophages and DC are from distinct lineages and that persistent recipient macrophages,although unlikely to initiate alloreactivity,may contribute to GVHD by sustaining the responses of previously activated T cells. View Publication

产品类型：

产品号#：

19155

19155RF

产品名：

Uhmann A et al. (SEP 2007) Blood 110 6 1814--23

The Hedgehog receptor Patched controls lymphoid lineage commitment.

A first step in hematopoiesis is the specification of the lymphoid and myeloid lineages from multipotent progenitor cells in the bone marrow. Using a conditional ablation strategy in adult mice,we show that this differentiation step requires Patched (Ptch),the cell surface-bound receptor for Hedgehog (Hh). In the absence of Ptch,the development of T- and B-lymphoid lineages is blocked at the level of the common lymphoid progenitor in the bone marrow. Consequently,the generation of peripheral T and B cells is abrogated. Cells of the myeloid lineage develop normally in Ptch mutant mice. Finally,adoptive transfer experiments identified the stromal cell compartment as a critical Ptch-dependent inducer of lymphoid versus myeloid lineage commitment. Our data show that Ptch acts as a master switch for proper diversification of hematopoietic stem cells in the adult organism. View Publication

产品类型：

产品号#：

03434

03444

产品名：

MethoCult™ GF M3434

Hoebeke I et al. (APR 2006) Blood 107 7 2879--81

Overexpression of HES-1 is not sufficient to impose T-cell differentiation on human hematopoietic stem cells.

By retroviral overexpression of the Notch-1 intracellular domain (ICN) in human CD34+ hematopoietic stem cells (HSCs),we have shown previously that Notch-1 signaling promotes the T-cell fate and inhibits the monocyte and B-cell fate in several in vitro and in vivo differentiation assays. Here,we investigated whether the effects of constitutively active Notch-1 can be mimicked by overexpression of its downstream target gene HES1. Upon HES-1 retroviral transduction,human CD34+ stem cells had a different outcome in the differentiation assays as compared to ICN-transduced cells. Although HES-1 induced a partial block in B-cell development,it did not inhibit monocyte development and did not promote T/NK-cell-lineage differentiation. On the contrary,a higher percentage of HES-1-transduced stem cells remained CD34+. These experiments indicate that HES-1 alone is not able to substitute for Notch-1 signaling to induce T-cell differentiation of human CD34+ hematopoietic stem cells. View Publication

产品类型：

产品号#：

18056

18056RF

产品名：

Curat CA et al. (MAY 2004) Diabetes 53 5 1285--92

From blood monocytes to adipose tissue-resident macrophages: induction of diapedesis by human mature adipocytes.

Obesity has been suggested to be a low-grade systemic inflammatory state,therefore we studied the interaction between human adipocytes and monocytes via adipose tissue (AT)-derived capillary endothelium. Cells composing the stroma-vascular fraction (SVF) of human ATs were characterized by fluorescence-activated cell sorter (FACS) analysis and two cell subsets (resident macrophages and endothelial cells [ECs]) were isolated using antibody-coupled microbeads. Media conditioned by mature adipocytes maintained in fibrin gels were applied to AT-derived ECs. Thereafter,the expression of endothelial adhesion molecules was analyzed as well as the adhesion and transmigration of human monocytes. FACS analysis showed that 11% of the SVF is composed of CD14(+)/CD31(+) cells,characterized as resident macrophages. A positive correlation was found between the BMI and the percentage of resident macrophages,suggesting that fat tissue growth is associated with a recruitment of blood monocytes. Incubation of AT-derived ECs with adipocyte-conditioned medium resulted in the upregulation of EC adhesion molecules and the increased chemotaxis of blood monocytes,an effect mimicked by recombinant human leptin. These results indicate that adipokines,such as leptin,activate ECs,leading to an enhanced diapedesis of blood monocytes,and suggesting that fat mass growth might be linked to inflammatory processes. View Publication

产品类型：

产品号#：

18058

18058RF

18056

18056RF

产品名：

产品手册

Reliable Antibodies for Your Research

产品类型：

品牌：

EasySep

产品号#：

60100

60100.1

60100AD

60100AD.1

60104

60104AD.1

60104AZ

60104AZ.1

60104BT

60104BT.1

60104FI.1

60104PE

60104PE.1

60106

60106.1

60106AZ

60106AZ.1

60106BT

60106FI

60106FI.1

60106PE

60106PE.1

产品名：

抗β-微管蛋白III抗体，克隆AA10

抗β-微管蛋白III抗体，克隆AA10，Alexa Fluor® 488

抗β-微管蛋白III抗体，clone AA10，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3

抗小鼠TCR Gamma/Delta抗体，clone GL3，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3，APC

抗小鼠TCR Gamma/Delta抗体，clone GL3，Biotin

抗小鼠TCR Gamma/Delta抗体，clone GL3，FITC

抗小鼠TCR Gamma/Delta抗体，clone GL3，PE

抗人CD71（转铁蛋白受体）抗体，clone OKT9

抗人CD71（转铁蛋白受体）抗体，clone OKT9，APC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，Biotin

抗人CD71（转铁蛋白受体）抗体，clone OKT9，FITC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，PE

技术公告

Endothelial Protein C Receptor (EPCR): A New Marker for Identification and Positive Selection of Mouse Hematopoietic Stem Cells

产品类型：

细胞类型：

造血干/祖细胞

产品号#：

17665

17665RF

17666

17666RF

17696

17696RF

产品名：

EasySep™小鼠生物素正选试剂盒II

RoboSep™ 小鼠生物素正选试剂盒II

EasySep™小鼠PE正选试剂盒II

RoboSep™ 小鼠PE正选试剂盒II

EasySep™小鼠PE正选试剂盒II

RoboSep™ 小鼠PE正选试剂盒II

Liu J et al. (NOV 2015) Nature Protocols 10 11 1842--59

Efficient delivery of nuclease proteins for genome editing in human stem cells and primary cells.

Targeted nucleases,including zinc-finger nucleases (ZFNs),transcription activator-like (TAL) effector nucleases (TALENs) and clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9),have provided researchers with the ability to manipulate nearly any genomic sequence in human cells and model organisms. However,realizing the full potential of these genome-modifying technologies requires their safe and efficient delivery into relevant cell types. Unlike methods that rely on expression from nucleic acids,the direct delivery of nuclease proteins to cells provides rapid action and fast turnover,leading to fewer off-target effects while maintaining high rates of targeted modification. These features make nuclease protein delivery particularly well suited for precision genome engineering. Here we describe procedures for implementing protein-based genome editing in human embryonic stem cells and primary cells. Protocols for the expression,purification and delivery of ZFN proteins,which are intrinsically cell-permeable; TALEN proteins,which can be internalized via conjugation with cell-penetrating peptide moieties; and Cas9 ribonucleoprotein,whose nucleofection into cells facilitates rapid induction of multiplexed modifications,are described,along with procedures for evaluating nuclease protein activity. Once they are constructed,nuclease proteins can be expressed and purified within 6 d,and they can be used to induce genomic modifications in human cells within 2 d. View Publication

产品类型：

产品号#：

07920

07922

100-0696

17952

17952RF

18000

19052

19052RF

85850

85857

产品名：

ACCUTASE™

EasySep™人CD4+ T细胞分离试剂盒

EasySep™人CD4+ T细胞分选试剂盒

RoboSep™ 人CD4+ T细胞分选试剂盒

EasySep™磁极

EasySep™人CD4+ T细胞富集试剂盒

RoboSep™ 人CD4+ T细胞富集试剂盒含滤芯吸头

mTeSR™1

Lian X et al. (NOV 2014) Stem cell reports 3 5 804--816

Efficient differentiation of human pluripotent stem cells to endothelial progenitors via small-molecule activation of WNT signaling.

Human pluripotent stem cell (hPSC)-derived endothelial cells and their progenitors may provide the means for vascularization of tissue-engineered constructs and can serve as models to study vascular development and disease. Here,we report a method to efficiently produce endothelial cells from hPSCs via GSK3 inhibition and culture in defined media to direct hPSC differentiation to CD34(+)CD31(+) endothelial progenitors. Exogenous vascular endothelial growth factor (VEGF) treatment was dispensable,and endothelial progenitor differentiation was β-catenin dependent. Furthermore,by clonal analysis,we showed that CD34(+)CD31(+)CD117(+)TIE-2(+) endothelial progenitors were multipotent,capable of differentiating into calponin-expressing smooth muscle cells and CD31(+)CD144(+)vWF(+)I-CAM1(+) endothelial cells. These endothelial cells were capable of 20 population doublings,formed tube-like structures,imported acetylated low-density lipoprotein,and maintained a dynamic barrier function. This study provides a rapid and efficient method for production of hPSC-derived endothelial progenitors and endothelial cells and identifies WNT/β-catenin signaling as a primary regulator for generating vascular cells from hPSCs. View Publication

产品类型：

产品号#：

73042

73044

85850

85857

产品名：

CHIR98014

mTeSR™1

Long T et al. (MAR 2014) Biomaterials 35 9 2752--9

The effect of mesenchymal stem cell sheets on structural allograft healing of critical sized femoral defects in mice.

Structural bone allografts are widely used in the clinic to treat critical sized bone defects,despite lacking the osteoinductive characteristics of live autografts. To address this,we generated revitalized structural allografts wrapped with mesenchymal stem/progenitor cell (MSC) sheets,which were produced by expanding primary syngenic bone marrow derived cells on temperature-responsive plates,as a tissue-engineered periosteum. In vitro assays demonstrated maintenance of the MSC phenotype in the sheets,suggesting that short-term culturing of MSC sheets is not detrimental. To test their efficacy in vivo,allografts wrapped with MSC sheets were transplanted into 4-mm murine femoral defects and compared to allografts with direct seeding of MSCs and allografts without cells. Evaluations consisted of X-ray plain radiography,3D microCT,histology,and biomechanical testing at 4- and 6-weeks post-surgery. Our findings demonstrate that MSC sheets induce prolonged cartilage formation at the graft-host junction and enhanced bone callus formation,as well as graft-host osteointegration. Moreover,a large periosteal callus was observed spanning the allografts with MSC sheets,which partially mimics live autograft healing. Finally,biomechanical testing showed a significant increase in the structural and functional properties of MSC sheet grafted femurs. Taken together,MSC sheets exhibit enhanced osteogenicity during critical sized bone defect repair,demonstrating the feasibility of this tissue engineering solution for massive allograft healing. View Publication

产品类型：

产品号#：

19771

产品名：

EasySep™ 小鼠间充质干/祖细胞富集试剂盒

Leung CG et al. (JUL 2007) The Journal of experimental medicine 204 7 1603--11

Requirements for survivin in terminal differentiation of erythroid cells and maintenance of hematopoietic stem and progenitor cells.

Survivin,which is the smallest member of the inhibitor of apoptosis protein (IAP) family,is a chromosomal passenger protein that mediates the spindle assembly checkpoint and cytokinesis,and also functions as an inhibitor of apoptosis. Frequently overexpressed in human cancers and not expressed in most adult tissues,survivin has been proposed as an attractive target for anticancer therapies and,in some cases,has even been touted as a cancer-specific gene. Survivin is,however,expressed in proliferating adult cells,including human hematopoietic stem cells,T-lymphocytes,and erythroid cells throughout their maturation. Therefore,it is unclear how survivin-targeted anticancer therapies would impact steady-state blood development. To address this question,we used a conditional gene-targeting strategy and abolished survivin expression from the hematopoietic compartment of mice. We show that inducible deletion of survivin leads to ablation of the bone marrow,with widespread loss of hematopoietic progenitors and rapid mortality. Surprisingly,heterozygous deletion of survivin causes defects in erythropoiesis in a subset of the animals,with a dramatic reduction in enucleated erythrocytes and the presence of immature megaloblastic erythroblasts. Our studies demonstrate that survivin is essential for steady-state hematopoiesis and survival of the adult,and further,that a high level of survivin expression is critical for proper erythroid differentiation. View Publication

产品类型：

产品号#：

19756

19756RF

产品名：

Yalcintepe L et al. (NOV 2006) Blood 108 10 3530--7

Expression of interleukin-3 receptor subunits on defined subpopulations of acute myeloid leukemia blasts predicts the cytotoxicity of diphtheria toxin interleukin-3 fusion protein against malignant progenitors that engraft in immunodeficient mice.

The interleukin-3 receptor (IL-3R) subunits are overexpressed on acute myeloid leukemia (AML) blasts compared with normal hematopoietic cells and are thus potential targets for novel therapeutic agents. Both fluorescence-activated cell sorter (FACS) analysis and quantitative real-time reverse transcription-polymerase chain reaction (QRT-PCR) were used to quantify expression of the IL-3Ralpha and beta(c) subunits on AML cells. QRT-PCR for both subunits was most predictive of killing of AML colony-forming cells (AML-CFCs) by diphtheria toxin-IL-3 fusion protein (DT(388)IL3). Among 19 patient samples,the relative level of the IL-3Ralpha was higher than the IL-3Rbeta(c) and highest in CD34(+)CD38(-)CD71(-) cells,enriched for candidate leukemia stem cells,compared with cell fractions depleted of such progenitors. Overall,the amount of IL-3Rbeta(c) subunit did not vary among sorted subpopulations. However,expression of both subunits varied by more than 10-fold among different AML samples for all subpopulations studied. The level of IL-3Rbeta(c) expression versus glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (set at 1000) ranged from 0.14 to 13.56 in CD34(+)CD38(-)CD71(-) cells from different samples; this value was correlated (r = .76,P = .05) with the ability of DT(388)IL3 to kill AML progenitors that engraft in beta(2)-microglobin-deficient nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice (n = 7). Thus,quantification of IL-3R subunit expression on AML blasts predicts the effectiveness IL-3R-targeted therapy in killing primitive leukemic progenitors. View Publication

产品类型：

产品号#：

18056

18056RF

产品名：

Hidalgo A et al. (JAN 2005) Blood 105 2 567--75

Enforced fucosylation of neonatal CD34+ cells generates selectin ligands that enhance the initial interactions with microvessels but not homing to bone marrow.

Hematopoietic progenitor/stem cell homing to the bone marrow requires the concerted action of several adhesion molecules. Endothelial P- and E-selectins play an important role in this process,but their ligands on a large subset of neonate-derived human CD34+ cells are absent,leading to a reduced ability to interact with the bone marrow (BM) microvasculature. We report here that this deficiency results from reduced alpha1,3-fucosyltransferase (FucT) expression and activity in these CD34+ cells. Incubation of CD34+ cells with recombinant human FucTVI rapidly corrected the deficiency in nonbinding CD34+ cells and further increased the density of ligands for both P- and E-selectins on all cord blood-derived CD34+ cells. Intravital microscopy studies revealed that these FucTVI-treated CD34+ cells displayed a marked enhancement in their initial interactions with the BM microvasculature,but unexpectedly,homing into the BM was not improved by FucTVI treatment. These data indicate that,although exogenous FucT enzyme activity can rapidly modulate selectin binding avidity of cord blood CD34+ cells,further studies are needed to understand how to translate a positive effect on progenitor cell adhesion in bone marrow microvessels into one that significantly influences migration and lodgement into the parenchyma. View Publication

产品类型：

产品号#：

18056

18056RF

产品名：

搜索结果: 'easysep'

Differential rates of replacement of human dermal dendritic cells and macrophages during hematopoietic stem cell transplantation.

The Hedgehog receptor Patched controls lymphoid lineage commitment.

Overexpression of HES-1 is not sufficient to impose T-cell differentiation on human hematopoietic stem cells.

From blood monocytes to adipose tissue-resident macrophages: induction of diapedesis by human mature adipocytes.

Efficient delivery of nuclease proteins for genome editing in human stem cells and primary cells.

Efficient differentiation of human pluripotent stem cells to endothelial progenitors via small-molecule activation of WNT signaling.

The effect of mesenchymal stem cell sheets on structural allograft healing of critical sized femoral defects in mice.

Requirements for survivin in terminal differentiation of erythroid cells and maintenance of hematopoietic stem and progenitor cells.

Expression of interleukin-3 receptor subunits on defined subpopulations of acute myeloid leukemia blasts predicts the cytotoxicity of diphtheria toxin interleukin-3 fusion protein against malignant progenitors that engraft in immunodeficient mice.

Enforced fucosylation of neonatal CD34+ cells generates selectin ligands that enhance the initial interactions with microvessels but not homing to bone marrow.

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