产品号 #15129_C
免疫密度负选试剂混合物
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总览
RosetteSep™人多发性骨髓瘤细胞富集抗体混合物用于通过负选从新鲜骨髓提取物中富集多发性骨髓瘤细胞（B细胞和浆细胞）。四聚体抗体复合物可识别CD2、CD14、CD33、CD41、CD45RA、CD66b以及红细胞（RBC）上的糖蛋白A，从而靶向去除非目的细胞。使用密度梯度离心液如Lymphoprep™（产品号 #18060）离心后 ，非目的细胞会与红细胞一起沉淀。纯化的多发性骨髓瘤细胞为血浆和密度梯度离心液的交界界面中高度富集的细胞。
亚型
细胞分选试剂盒
细胞类型
B 细胞，血浆
种属
人
样本来源
Bone Marrow
筛选方法
Negative
应用
细胞分选
品牌
RosetteSep
研究领域
癌症，免疫
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (4)
Frequently Asked Questions
Publications (11)
p53-related protein kinase confers poor prognosis and represents a novel therapeutic target in multiple myeloma. Blood 2017 JAN
Abstract
p53-related protein kinase (TP53RK, also known as PRPK) is an upstream kinase which phosphorylates (Ser15) and mediates p53 activity. Here we show that TP53RK confers poor prognosis in MM patients; and conversely, that TP53RK knockdown inhibits p53 phosphorylation and triggers multiple myeloma (MM) cell apoptosis, associated with downregulation of c-Myc and E2F-1-mediated upregulation of pro-apoptotic Bim. We further demonstrate that TP53RK downregulation also triggers growth inhibition in p53-deficient (KMS-11) and p53-mutant (U266) MM cell lines, and identify novel downstream targets of TP53RK including ribonucleotide reductase-1, telomerase reverse transcriptase, and cyclin dependent kinase inhibitor 2C (CDKN2C). Our previous studies showed that immunomodulatory drugs (IMiDs) downregulate p21 and trigger apoptosis in wt-p53 MM.1S cells, Importantly we here demonstrate by pull-down, nuclear magnetic resonance spectroscopy, differential scanning fluorimetry, and isothermal titration calorimetry, that IMiDs bind and inhibit TP53RK, with biologic sequelae similar to TP53RK knockdown. Our studies therefore demonstrate that either genetic or pharmacological inhibition of TP53RK triggers MM cell apoptosis via both p53-Myc axis-dependent and -independent pathways, validating TP53RK as a novel therapeutic target in patients with poor prognosis MM.
Discovery of selective small-molecule HDAC6 inhibitor for overcoming proteasome inhibitor resistance in multiple myeloma. Proceedings of the National Academy of Sciences of the United States of America 2016 OCT
Abstract
Multiple myeloma (MM) has proven clinically susceptible to modulation of pathways of protein homeostasis. Blockade of proteasomal degradation of polyubiquitinated misfolded proteins by the proteasome inhibitor bortezomib (BTZ) achieves responses and prolongs survival in MM, but long-term treatment with BTZ leads to drug-resistant relapse in most patients. In a proof-of-concept study, we previously demonstrated that blocking aggresomal breakdown of polyubiquitinated misfolded proteins with the histone deacetylase 6 (HDAC6) inhibitor tubacin enhances BTZ-induced cytotoxicity in MM cells in vitro. However, these foundational studies were limited by the pharmacologic liabilities of tubacin as a chemical probe with only in vitro utility. Emerging from a focused library synthesis, a potent, selective, and bioavailable HDAC6 inhibitor, WT161, was created to study the mechanism of action of HDAC6 inhibition in MM alone and in combination with BTZ. WT161 in combination with BTZ triggers significant accumulation of polyubiquitinated proteins and cell stress, followed by caspase activation and apoptosis. More importantly, this combination treatment was effective in BTZ-resistant cells and in the presence of bone marrow stromal cells, which have been shown to mediate MM cell drug resistance. The activity of WT161 was confirmed in our human MM cell xenograft mouse model and established the framework for clinical trials of the combination treatment to improve patient outcomes in MM.
Immuno-targeting the multifunctional CD38 using nanobody. Scientific reports 2016
Abstract
CD38, as a cell surface antigen is highly expressed in several hematologic malignancies including multiple myeloma (MM) and has been proven to be a good target for immunotherapy of the disease. CD38 is also a signaling enzyme responsible for the metabolism of two novel calcium messenger molecules. To be able to target this multifunctional protein, we generated a series of nanobodies against CD38 with high affinities. Crystal structures of the complexes of CD38 with the nanobodies were solved, identifying three separate epitopes on the carboxyl domain. Chromobodies, engineered by tagging the nanobody with fluorescence proteins, provide fast, simple and versatile tools for quantifying CD38 expression. Results confirmed that CD38 was highly expressed in malignant MM cells compared with normal white blood cells. The immunotoxin constructed by splicing the nanobody with a bacterial toxin, PE38 shows highly selective cytotoxicity against patient-derived MM cells as well as the cell lines, with half maximal effective concentration reaching as low as 10(-11) molar. The effectiveness of the immunotoxin can be further increased by stimulating CD38 expression using retinoid acid. These results set the stage for the development of clinical therapeutics as well as diagnostic screening for myeloma.
更多信息
| Species | Human |
|---|---|
| Sample Source | Bone Marrow |
| Selection Method | Negative |
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