EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #03436_C
含重组细胞因子（包括EPO）的小鼠红细胞祖细胞无血清甲基纤维素培养基
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总览
MethoCult™ SF M3436经过优化，适用于小鼠骨髓、胎肝、脾脏、外周血和纯化细胞的集落形成单位（CFU）分析时原始红系祖细胞（BFU-E）的生长和计数。MethoCult™ SF M3436不支持粒细胞-巨噬细胞祖细胞（CFU-GM、CFU-G和CFU-M）或多能粒细胞、红系、巨噬细胞、巨核细胞祖细胞（CFU-GEMM）的生长。本产品不含血清，与用于小鼠骨髓CFU分析自动化集落计数的STEMvision™软件兼容。MethoCult™ SF M3436也可用于大鼠骨髓细胞CFU分析时BFU-E的培养和计数。点击此处了解有关进行CFU检测的常见问题（FAQ）。
包含
• 含甲基纤维素的Iscove's MDM
• 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
• 细胞因子（包括重组人促红细胞生成素 [EPO]）
• 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、大鼠
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
无血清
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 (8)
常见问题
文献 (2)
Genomic subtyping and therapeutic targeting of acute erythroleukemia. Nature genetics 2019
Abstract
Acute erythroid leukemia (AEL) is a high-risk leukemia of poorly understood genetic basis, with controversy regarding diagnosis in the spectrum of myelodysplasia and myeloid leukemia. We compared genomic features of 159 childhood and adult AEL cases with non-AEL myeloid disorders and defined five age-related subgroups with distinct transcriptional profiles: adult, TP53 mutated; NPM1 mutated; KMT2A mutated/rearranged; adult, DDX41 mutated; and pediatric, NUP98 rearranged. Genomic features influenced outcome, with NPM1 mutations and HOXB9 overexpression being associated with a favorable prognosis and TP53, FLT3 or RB1 alterations associated with poor survival. Targetable signaling mutations were present in 45{\%} of cases and included recurrent mutations of ALK and NTRK1, the latter of which drives erythroid leukemogenesis sensitive to TRK inhibition. This genomic landscape of AEL provides the framework for accurate diagnosis and risk stratification of this disease, and the rationale for testing targeted therapies in this high-risk leukemia.
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.
更多信息
| 种属 | Mouse, Rat |
|---|---|
| Contains | • Methylcellulose in Iscove's MDM • Bovine serum albumin • Recombinant human insulin • Human transferrin (iron-saturated) • 2-Mercaptoethanol • Cytokines (including recombinant human erythropoietin [EPO]) • Supplements |
| 配方类别 | Serum-Free |
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