EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #03534_C
含重组细胞因子（不含促红细胞生成素 [EPO]）的甲基纤维素培养基，用于小鼠髓系祖细胞
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总览
MethoCult™GF M3534针对在小鼠骨髓、脾脏、外周血和胎肝细胞集落形成单位（CFU）检测中粒细胞-巨噬细胞祖细胞（CFU-GM、CFU-G和CFU-M）的生长和计数进行优化。MethoCult™M3534不含促红细胞生成素（EPO），因此不支持红系祖细胞（BFU-E和CFU-E）。该配方与STEMvision™软件兼容，用于小鼠骨髓CFU检测的自动集落计数。
参阅关于进行CFU实验的常见问题和解答（FAQ）。
包含
• 含甲基纤维素的Iscove's MDM
• 胎牛血清
• 牛血清白蛋白
• 重组人胰岛素
• 人转铁蛋白（铁饱和）
• 2-巯基乙醇
• 重组小鼠干细胞因子 (SCF)
• 重组小鼠白细胞介素3 (IL-3)
• 重组人白细胞介素6 (IL-6)
• 添加物
分类
半固体培养基，专用培养基
细胞类型
造血干/祖细胞
种属
小鼠
应用
细胞培养，克隆筛选，功能学筛选
品牌
MethoCult
研究领域
药物发现和毒理检测，干细胞生物学
制剂类别
甲基纤维素基
实验数据
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 (2)
文献 (21)
Inhibition of the TGF-beta receptor I kinase promotes hematopoiesis in MDS.
Blood 2008 OCT
Abstract
MDS is characterized by ineffective hematopoiesis that leads to peripheral cytopenias. Development of effective treatments has been impeded by limited insight into pathogenic pathways governing dysplastic growth of hematopoietic progenitors. We demonstrate that smad2,a downstream mediator of transforming growth factor-beta (TGF-beta) receptor I kinase (TBRI) activation,is constitutively activated in MDS bone marrow (BM) precursors and is overexpressed in gene expression profiles of MDS CD34(+) cells,providing direct evidence of overactivation of TGF-beta pathway in this disease. Suppression of the TGF-beta signaling by lentiviral shRNA-mediated down-regulation of TBRI leads to in vitro enhancement of hematopoiesis in MDS progenitors. Pharmacologic inhibition of TBRI (alk5) kinase by a small molecule inhibitor,SD-208,inhibits smad2 activation in hematopoietic progenitors,suppresses TGF-beta-mediated gene activation in BM stromal cells,and reverses TGF-beta-mediated cell-cycle arrest in BM CD34(+) cells. Furthermore,SD-208 treatment alleviates anemia and stimulates hematopoiesis in vivo in a novel murine model of bone marrow failure generated by constitutive hepatic expression of TGF-beta1. Moreover,in vitro pharmacologic inhibition of TBRI kinase leads to enhancement of hematopoiesis in varied morphologic MDS subtypes. These data directly implicate TGF-beta signaling in the pathobiology of ineffective hematopoiesis and identify TBRI as a potential therapeutic target in low-risk MDS.
Failure of carrageenan to affect graft-versus-host reactivity in the rat.
Transplantation 1975 NOV
Abstract
Fanconi anemia (FA) is an inherited recessive DNA repair disorder mainly characterized by bone marrow failure and cancer predisposition. Studies in mosaic FA patients have shown that reversion of one inherited germ-line mutation resulting in a functional allele in one or a few hematopoietic stem cells (HSCs) can lead to the proliferation advantage of corrected cells,thus over time normalizing the hematologic status of the patient. In contrast to these observations,it is still unclear whether ex vivo genetic correction of FA HSCs also provides a similar proliferation advantage to FA HSCs. Using an FA mouse model with a marked hematopoietic phenotype,the FA-D1 (Brca2(Delta27/Delta27)) mice,we demonstrate that the lentivirus-mediated gene therapy of FA HSCs results in the progressive expansion of genetically corrected clones in mild-conditioned FA-D1 recipients. Consistent with these data,hematopoietic progenitors from FA recipients progressively became mitomycin C resistant and their chromosomal instability was reverted. No evidence of myelodysplasia,leukemias,or abnormal clonal repopulation was observed at multiple time points in primary or secondary recipients. Our results demonstrate that ectopic expression of BRCA2 confers a beneficial in vivo proliferation advantage to FA-D1 HSCs that enables the full hematopoietic repopulation of FA recipients with genetically corrected cells.
DYRK3 dual-specificity kinase attenuates erythropoiesis during anemia.
The Journal of biological chemistry 2008 DEC
Abstract
During anemia erythropoiesis is bolstered by several factors including KIT ligand,oncostatin-M,glucocorticoids,and erythropoietin. Less is understood concerning factors that limit this process. Experiments performed using dual-specificity tyrosine-regulated kinase-3 (DYRK3) knock-out and transgenic mice reveal that erythropoiesis is attenuated selectively during anemia. DYRK3 is restricted to erythroid progenitor cells and testes. DYRK3-/- mice exhibited essentially normal hematological profiles at steady state and reproduced normally. In response to hemolytic anemia,however,reticulocyte production increased severalfold due to DYRK3 deficiency. During 5-fluorouracil-induced anemia,both reticulocyte and red cell formation in DYRK3-/- mice were elevated. In short term transplant experiments,DYRK3-/- progenitors also supported enhanced erythroblast formation,and erythropoietic advantages due to DYRK3-deficiency also were observed in 5-fluorouracil-treated mice expressing a compromised erythropoietin receptor EPOR-HM allele. As analyzed ex vivo,DYRK3-/- erythroblasts exhibited enhanced CD71posTer119pos cell formation and 3HdT incorporation. Transgenic pA2gata1-DYRK3 mice,in contrast,produced fewer reticulocytes during hemolytic anemia,and pA2gata1-DYRK3 progenitors were compromised in late pro-erythroblast formation ex vivo. Finally,as studied in erythroid K562 cells,DYRK3 proved to effectively inhibit NFAT (nuclear factor of activated T cells) transcriptional response pathways and to co-immunoprecipitate with NFATc3. Findings indicate that DYRK3 attenuates (and possibly apportions) red cell production selectively during anemia.
更多信息
| 物种 | 小鼠 |
|---|---|
| Contains | • Methylcellulose in Iscove's MDM • Fetal bovine serum • Bovine serum albumin • Recombinant human insulin • Human transferrin (iron-saturated) • 2-Mercaptoethanol • Recombinant mouse stem cell factor (SCF) • Recombinant mouse interleukin 3 (IL-3) • Recomb |
| 配方 | 甲基纤维素基 |
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