RoboSep™- S

全自动细胞分选仪、可同时或依次进行多达四次EasySep™细胞分选。

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产品号 #（选择产品）

产品号 #21000_C

全自动细胞分选仪器

产品优势

减少手动操作时间和用户操作差异
最大程度减少样本处理和接触危险病原体的风险
使用正选或负选方案、从多种来源和规格的样本中分离几乎任何类型的细胞
通过定制化工作流程、分离用于特殊或非标准应用的目标细胞

产品组分包括

RoboSep™-S 主机（产品号 #21001）
4个“The Big Easy” EasySep™ 磁极（产品号 #18001）
RoboSep™ 服务包（产品号 #20101）
4x RoboSep™ 试管套件（产品号 #20155）
RoboSep™ 吸头抛光剂（产品号 #20119）
USB 闪存盘（产品号 #20112）
RoboSep™-S 用户参考手册（产品号 #29792）
RoboSep™ 快速入门指南（产品号 #28943）
一年保修（产品号 #21200)

立即询价

总览

RoboSep™-S可实现全自动化细胞处理和分选，最大程度地减少样本处理，消除交叉污染，并减少手动操作时间。RoboSep™-S采用EasySep™无柱细胞分选技术，可执行所有必要步骤，通过磁珠标记和正选或负选，从多达四个样本中分离几乎所有类型的细胞。这款易使用的台式系统无需日常维护或清洁，十多年来一直深受全球科研人员的信赖。

RoboSep™-S可从各种不同物种、组织来源或规格的样本中分离目标细胞。分选后的目标细胞即可用于下游免疫学和诊断研究应用。终端使用人需要负责验证该平台是否适用于下游检测。使用EasySep™人细胞外囊泡正选试剂盒，也可实现自动化分离细胞外囊泡 (EV) 。如需了解RoboSep™-S如何优化您的特定细胞分选流程，请申请现场演示。

此外，我们还提供租赁方案和服务计划。如需了解更多信息，请浏览RoboSep™-S的仪器服务，包括保修范围、软件更新和其他服务包，或下载我们的仪器服务手册。无论您是为单个实验步骤引入仪器，还是连接多个实验体系，STEMCELLTechnologies都能提供适用于您的实验室仪器，这些仪器可无缝衔接至各种基于细胞的工作流程中。

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。

Document Type

Product Name

Catalog #

Lot #

Language

Document Type

Quick Start Procedure

Product Name

RoboSep™-S

Catalog #

21000

Lot #

All

Language

English

Document Type

Technical Manual

Product Name

RoboSep™-S

Catalog #

21000

Lot #

All

Language

English

文献 (67)

Thymoglobulin targets multiple plasma cell antigens and has in vitro and in vivo activity in multiple myeloma. Timm MM et al. Leukemia 2006 OCT

Abstract

Multiple myeloma is characterized by the proliferation of clonal plasma cells that have a heterogeneous expression of various cell surface markers,precluding successful use of monoclonal antibodies for therapeutic targeting of the tumor cell. Thymoglobulin (rabbit-derived polyclonal anti-thymocyte globulin),by virtue of its method of preparation,contains antibodies against several B-cell and plasma cell antigens and offers an attractive option for immunotherapy of myeloma. Here,we demonstrate potent anti-myeloma activity of the rabbit anti-thymocyte globulin preparation Thymoglobulin in vitro and in vivo in an animal model of myeloma. Thymoglobulin was able to induce dose- and time-dependent apoptosis of several myeloma cell lines,including those resistant to conventional anti-myeloma agents. Importantly,the anti-myeloma activity was preserved even when myeloma cells were grown with different cytokines demonstrating the ability to overcome microenvironment-mediated resistance. Thymoglobulin induced apoptosis of freshly isolated primary myeloma cells from patients. Using a competitive flow cytometric analysis,we were able to identify the potential antigen targets for Thymoglobulin preparation. Finally,in a plasmacytoma mouse model of myeloma,Thymoglobulin delayed the tumor growth in a dose-dependent manner providing convincing evidence for continued evaluation of this agent in the clinic in patients with myeloma,either alone or in combination with other agents.

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Chaetocin: a promising new antimyeloma agent with in vitro and in vivo activity mediated via imposition of oxidative stress. Isham CR et al. Blood 2007 MAR

Abstract

Chaetocin,a thiodioxopiperazine natural product previously unreported to have anticancer effects,was found to have potent antimyeloma activity in IL-6-dependent and -independent myeloma cell lines in freshly collected sorted and unsorted patient CD138(+) myeloma cells and in vivo. Chaetocin largely spares matched normal CD138(-) patient bone marrow leukocytes,normal B cells,and neoplastic B-CLL (chronic lymphocytic leukemia) cells,indicating a high degree of selectivity even in closely lineage-related B cells. Furthermore,chaetocin displays superior ex vivo antimyeloma activity and selectivity than doxorubicin and dexamethasone,and dexamethasone- or doxorubicin-resistant myeloma cell lines are largely non-cross-resistant to chaetocin. Mechanistically,chaetocin is dramatically accumulated in cancer cells via a process inhibited by glutathione and requiring intact/unreduced disulfides for uptake. Once inside the cell,its anticancer activity appears mediated primarily through the imposition of oxidative stress and consequent apoptosis induction. Moreover,the selective antimyeloma effects of chaetocin appear not to reflect differential intracellular accumulation of chaetocin but,instead,heightened sensitivity of myeloma cells to the cytotoxic effects of imposed oxidative stress. Considered collectively,chaetocin appears to represent a promising agent for further study as a potential antimyeloma therapeutic.

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17beta-estradiol downregulates interferon regulatory factor-1 in murine splenocytes. Lengi AJ et al. Journal of molecular endocrinology 2006 DEC

Abstract

Interferon regulatory factor-1 (IRF-1) is an important transcription factor that mediates interferon-gamma (IFN-gamma)-induced cell-signaling events. In this study,we examined whether 17beta-estradiol alters IRF-1 in splenic lymphocytes,in view of the immunomodulatory effects of this natural female sex hormone including its ability to alter IFN-gamma levels. We find that IRF-1 expression is markedly downregulated in splenocytes or purified T-cells from estrogen-treated mice at all time points studied when compared with their placebo counterparts. This decrease in IRF-1 in splenocytes from estrogen-treated mice is neither due to upregulation of IRF-1-interfering proteins (nucleophosmin or signal transducer and activator of transcription (STAT)-5) nor due to alternatively spliced IRF-1 mRNA. Given that IFN-gamma is a potent inducer of IRF-1,direct addition of recombinant IFN-gamma to splenocytes from either wild-type or IFN-gamma-knockout mice,or the addition of recombinant IFN-gamma to purified T-cells,was expected to stimulate IRF-1 expression. However,robust expression of IRF-1 in cells from estrogen-treated mice was not seen,unlike what was observed in cells from placebo-treated mice. Diminished IFN-gamma induction of IRF-1 in cells from estrogen-treated mice was noticed despite comparable phosphorylated STAT-1 activation. These studies are the first to show that estrogen regulates IFN-gamma-inducible IRF-1 in lymphoid cells,a finding that may have implications to IFN-gamma-regulated immune and vascular diseases.

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