EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #03630_C
用于小鼠前B淋巴祖细胞的甲基纤维素培养基
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总览
MethoCult™ M3630经过优化，适用于小鼠骨髓集落形成单位（CFU）分析和Whitlock-Witte长期培养时的小鼠前B淋巴样祖细胞的生长和计数。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
• 胎牛血清
• 2-巯基乙醇
• 重组人白细胞介素7 (IL-7)
• 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
药物发现和毒性检测，干细胞生物学
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)
常见问题
文献 (22)
Epstein-Barr virus LMP2A interferes with global transcription factor regulation when expressed during B-lymphocyte development.
Journal of virology 2003 JAN
Abstract
Epstein-Barr virus (EBV) is associated with the development of malignant lymphomas and lymphoproliferative disorders in immunocompromised individuals. The LMP2A protein of EBV is thought to play a central role in this process by allowing the virus to persist in latently infected B lymphocytes. We have demonstrated that LMP2A,when expressed in B cells of transgenic mice,allows normal B-cell developmental checkpoints to be bypassed. To identify cellular genes targeted by LMP2A that are involved in this process,we have utilized DNA microarrays to compare gene transcription in B cells from wild-type versus LMP2A transgenic mice. In B cells from LMP2A transgenic mice,we observed decreased expression of many genes associated with normal B-cell development as well as reduced levels of the transcription factors that regulate their expression. In particular,expression of the transcription factor E2A was down-regulated in bone marrow and splenic B cells. Furthermore,E2A activity was inhibited in these cells as determined by decreased DNA binding and reduced expression of its target genes,including the transcription factors early B-cell factor and Pax-5. Expression of two E2A inhibitors,Id2 and SCL,was up-regulated in splenic B cells expressing LMP2A,suggesting a possible mechanism for E2A inhibition. These results indicate that LMP2A deregulates transcription factor expression and activity in developing B cells,and this likely allows for a bypass of normal signaling events required for proper B-cell development. The ability of LMP2A to interfere with B-cell transcription factor regulation has important implications regarding its role in EBV latency.
Induction of acute myeloid leukemia in mice by the human leukemia-specific fusion gene NUP98-HOXD13 in concert with Meis1.
Blood 2003 JUN
Abstract
HOX genes,notably members of the HOXA cluster,and HOX cofactors have increasingly been linked to human leukemia. Intriguingly,HOXD13,a member of the HOXD cluster not normally expressed in hematopoietic cells,was recently identified as a partner of NUP98 in a t(2;11) translocation associated with t-AML/MDS. We have now tested directly the leukemogenic potential of the NUP98-HOXD13 t(2; 11) fusion gene in the murine hematopoietic model. NUP98-HOXD13 strongly promoted growth and impaired differentiation of early hematopoietic progenitor cells in vitro; this effect was dependent on the NUP98 portion and an intact HOXD13 homeodomain. Expression of the NUP98-HOXD13 fusion gene in vivo resulted in a partial impairment of lymphopoiesis but did not induce evident hematologic disease until late after transplantation (more than 5 months),when some mice developed a myeloproliferative-like disease. In contrast,mice transplanted with bone marrow (BM) cells cotransduced with NUP98-HOXD13 and the HOX cofactor Meis1 rapidly developed lethal and transplantable acute myeloid leukemia (AML),with a median disease onset of 75 days. In summary,this study demonstrates that NUP98-HOXD13 can be directly implicated in the molecular process leading to leukemic transformation,and it supports a model in which the transforming properties of NUP98-HOXD13 are mediated through HOX-dependent pathways.
Lymphodepletion in the ApcMin/+ mouse model of intestinal tumorigenesis.
Blood 2004 FEB
Abstract
Germ line mutations in the Adenomatous polyposis coli tumor suppressor gene cause a hereditary form of intestinal tumorigenesis in both mice and man. Here we show that in Apc(Min/+) mice,which carry a heterozygous germ line mutation at codon 850 of Apc,there is progressive loss of immature and mature thymocytes from approximately 80 days of age with complete regression of the thymus by 120 days. In addition,Apc(Min/+) mice show parallel depletion of splenic natural killer (NK) cells,immature B cells,and B progenitor cells in bone marrow due to complete loss of interleukin 7 (IL-7)-dependent B-cell progenitors. Using bone marrow transplantation experiments into wild-type recipients,we have shown that the capacity of transplanted Apc(Min/+) bone marrow cells for T- and B-cell development appears normal. In contrast,although the Apc(Min/+) bone marrow microenvironment supported short-term reconstitution with wild-type bone marrow,Apc(Min/+) animals that received transplants subsequently underwent lymphodepletion. Fibroblast colony-forming unit (CFU-F) colony assays revealed a significant reduction in colony-forming mesenchymal progenitor cells in the bone marrow of Apc(Min/+) mice compared with wild-type animals prior to the onset of lymphodepletion. This suggests that an altered bone marrow microenvironment may account for the selective lymphocyte depletion observed in this model of familial adenomatous polyposis.
更多信息
| 物种 | 小鼠 |
|---|---|
| Contains | • Methylcellulose in Iscove's MDM • Fetal bovine serum • 2-Mercaptoethanol • Recombinant human interleukin 7 (IL-7) • Supplements |
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