EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #02697_C
人造血细胞扩增的无血清培养补充物
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总览
StemSpan™ CC110含有多种早期作用的重组人（rh）细胞因子，旨在支持人造血细胞的扩增。该产品以100X浓缩液的形式提供。当添加到无血清培养基中时，StemSpan™ CC110可促进从人脐带血和骨髓中分离的CD34+细胞的扩增。StemSpan™ CC110刺激CD34+ 细胞的扩增效果与StemSpan™ CC100类似，但具有更高的纯度，适用于短期培养以激活干细胞和未成熟祖细胞的循环，而不一定促进后期祖细胞的增殖和分化。我们建议将StemSpan™ CC110与以下任意StemSpan™培养基搭配使用：•StemSpan™ SFEM（产品号 #09600）•StemSpan™ SFEM II（产品号 #09605）•StemSpan™-XF（产品号 #100-0073）•StemSpan™-AOF（产品号 #100-0130）
包含
• 重组人FMS样酪氨酸激酶3配体（Flt3L）
• 重组人干细胞因子（SCF）
• 重组人血小板生成素（TPO）
分类
添加剂
细胞类型
造血干/祖细胞
种属
人
应用
细胞培养，扩增
品牌
StemSpan
研究领域
干细胞生物学，移植研究
制剂类别
无血清
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。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (6)
文献 (13)
Selection-free genome editing of the sickle mutation in human adult hematopoietic stem/progenitor cells. Science translational medicine 2016 OCT
Abstract
Genetic diseases of blood cells are prime candidates for treatment through ex vivo gene editing of CD34+ hematopoietic stem/progenitor cells (HSPCs), and a variety of technologies have been proposed to treat these disorders. Sickle cell disease (SCD) is a recessive genetic disorder caused by a single-nucleotide polymorphism in the $\beta$-globin gene (HBB). Sickle hemoglobin damages erythrocytes, causing vasoocclusion, severe pain, progressive organ damage, and premature death. We optimize design and delivery parameters of a ribonucleoprotein (RNP) complex comprising Cas9 protein and unmodified single guide RNA, together with a single-stranded DNA oligonucleotide donor (ssODN), to enable efficient replacement of the SCD mutation in human HSPCs. Corrected HSPCs from SCD patients produced less sickle hemoglobin RNA and protein and correspondingly increased wild-type hemoglobin when differentiated into erythroblasts. When engrafted into immunocompromised mice, ex vivo treated human HSPCs maintain SCD gene edits throughout 16 weeks at a level likely to have clinical benefit. These results demonstrate that an accessible approach combining Cas9 RNP with an ssODN can mediate efficient HSPC genome editing, enables investigator-led exploration of gene editing reagents in primary hematopoietic stem cells, and suggests a path toward the development of new gene editing treatments for SCD and other hematopoietic diseases.
Directed evolution of a recombinase that excises the provirus of most HIV-1 primary isolates with high specificity. Nature Biotechnology 2016 APR
Abstract
Current combination antiretroviral therapies (cART) efficiently suppress HIV-1 reproduction in humans, but the virus persists as integrated proviral reservoirs in small numbers of cells. To generate an antiviral agent capable of eradicating the provirus from infected cells, we employed 145 cycles of substrate-linked directed evolution to evolve a recombinase (Brec1) that site-specifically recognizes a 34-bp sequence present in the long terminal repeats (LTRs) of the majority of the clinically relevant HIV-1 strains and subtypes. Brec1 efficiently, precisely and safely removes the integrated provirus from infected cells and is efficacious on clinical HIV-1 isolates in vitro and in vivo, including in mice humanized with patient-derived cells. Our data suggest that Brec1 has potential for clinical application as a curative HIV-1 therapy.
PPAR-α and glucocorticoid receptor synergize to promote erythroid progenitor self-renewal. Nature 2015 JUN
Abstract
Many acute and chronic anaemias, including haemolysis, sepsis and genetic bone marrow failure diseases such as Diamond-Blackfan anaemia, are not treatable with erythropoietin (Epo), because the colony-forming unit erythroid progenitors (CFU-Es) that respond to Epo are either too few in number or are not sensitive enough to Epo to maintain sufficient red blood cell production. Treatment of these anaemias requires a drug that acts at an earlier stage of red cell formation and enhances the formation of Epo-sensitive CFU-E progenitors. Recently, we showed that glucocorticoids specifically stimulate self-renewal of an early erythroid progenitor, burst-forming unit erythroid (BFU-E), and increase the production of terminally differentiated erythroid cells. Here we show that activation of the peroxisome proliferator-activated receptor α (PPAR-α) by the PPAR-α agonists GW7647 and fenofibrate synergizes with the glucocorticoid receptor (GR) to promote BFU-E self-renewal. Over time these agonists greatly increase production of mature red blood cells in cultures of both mouse fetal liver BFU-Es and mobilized human adult CD34(+) peripheral blood progenitors, with a new and effective culture system being used for the human cells that generates normal enucleated reticulocytes. Although Ppara(-/-) mice show no haematological difference from wild-type mice in both normal and phenylhydrazine (PHZ)-induced stress erythropoiesis, PPAR-α agonists facilitate recovery of wild-type but not Ppara(-/-) mice from PHZ-induced acute haemolytic anaemia. We also show that PPAR-α alleviates anaemia in a mouse model of chronic anaemia. Finally, both in control and corticosteroid-treated BFU-E cells, PPAR-α co-occupies many chromatin sites with GR; when activated by PPAR-α agonists, additional PPAR-α is recruited to GR-adjacent sites and presumably facilitates GR-dependent BFU-E self-renewal. Our discovery of the role of PPAR-α agonists in stimulating self-renewal of early erythroid progenitor cells suggests that the clinically tested PPAR-α agonists we used may improve the efficacy of corticosteroids in treating Epo-resistant anaemias.
更多信息
| 种属 | Human |
|---|---|
| Contains | • Recombinant human fms-like tyrosine kinase 3 ligand (Flt3L) • Recombinant human stem cell factor (SCF) • Recombinant human thrombopoietin (TPO) |
| 配方类别 | Serum-Free |
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