EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #03814_C
半固体甲基纤维素培养基，用于选择和克隆悬浮适应细胞和贴壁细胞（含血清）
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总览
ClonaCell™-TCS 培养基是一款含血清、基于甲基纤维素的半固体培养基，适用于筛选和克隆多种悬浮适应性细胞株，包括 CHO-S 和杂交瘤细胞。该培养基亦可用于部分贴壁生长、在血清条件下培养的细胞系的半固体克隆培养，如 CHO-K1、BHK-1 和 HEK-293 等。该培养基含经过预筛选的胎牛血清（FBS）和牛血清白蛋白（BSA），可支持多种细胞类型的稳健生长。ClonaCell™-TCS 培养基不含筛选剂。
半固体克隆培养的优势：
•单个细胞悬浮于高黏度培养基中，形成物理分离、独立的克隆集落，便于挑取；
•相较于极限稀释法，使用该方法可更快速、节省资源地获得单克隆细胞系；
•在黏性培养基中，具有不同生长速率和产量的多样性克隆均可形成独立集落，从而更易于筛选出稀有的高产克隆。相比液体批量培养，半固体培养支持同时进行筛选和克隆，提高高表达克隆的获取效率。
包含
• IMDM (Iscove's改良杜氏培养基)
• 甲基纤维素
• 预筛选血清
• 牛血清白蛋白
• 2-巯基乙醇
• 酚红
• L-谷氨酰胺
• 其他成分
分类
半固体培养基，专用培养基
细胞类型
CHO细胞，HEK-293细胞（人胚肾293细胞），杂交瘤细胞，其它细胞系
种属
小鼠，其它细胞系
应用
细胞培养，半固体克隆
品牌
ClonaCell
研究领域
抗体制备，细胞系制备，杂交瘤制备
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 (12)
The T-cell leukemia-associated ribosomal RPL10 R98S mutation enhances JAK-STAT signaling. Leukemia 2018 MAR
Abstract
Several somatic ribosome defects have recently been discovered in cancer, yet their oncogenic mechanisms remain poorly understood. Here we investigated the pathogenic role of the recurrent R98S mutation in ribosomal protein L10 (RPL10 R98S) found in T-cell acute lymphoblastic leukemia (T-ALL). The JAK-STAT signaling pathway is a critical controller of cellular proliferation and survival. A proteome screen revealed overexpression of several Jak-Stat signaling proteins in engineered RPL10 R98S mouse lymphoid cells, which we confirmed in hematopoietic cells from transgenic Rpl10 R98S mice and T-ALL xenograft samples. RPL10 R98S expressing cells displayed JAK-STAT pathway hyper-activation upon cytokine stimulation, as well as increased sensitivity to clinically used JAK-STAT inhibitors like pimozide. A mutually exclusive mutation pattern between RPL10 R98S and JAK-STAT mutations in T-ALL patients further suggests that RPL10 R98S functionally mimics JAK-STAT activation. Mechanistically, besides transcriptional changes, RPL10 R98S caused reduction of apparent programmed ribosomal frameshifting at several ribosomal frameshift signals in mouse and human Jak-Stat genes, as well as decreased Jak1 degradation. Of further medical interest, RPL10 R98S cells showed reduced proteasome activity and enhanced sensitivity to clinical proteasome inhibitors. Collectively, we describe modulation of the JAK-STAT cascade as a novel cancer-promoting activity of a ribosomal mutation, and expand the relevance of this cascade in leukemia.
DNMT3A mutations promote anthracycline resistance in acute myeloid leukemia via impaired nucleosome remodeling. Nature Medicine 2016 NOV
Abstract
Although the majority of patients with acute myeloid leukemia (AML) initially respond to chemotherapy, many of them subsequently relapse, and the mechanistic basis for AML persistence following chemotherapy has not been determined. Recurrent somatic mutations in DNA methyltransferase 3A (DNMT3A), most frequently at arginine 882 (DNMT3A(R882)), have been observed in AML and in individuals with clonal hematopoiesis in the absence of leukemic transformation. Patients with DNMT3A(R882) AML have an inferior outcome when treated with standard-dose daunorubicin-based induction chemotherapy, suggesting that DNMT3A(R882) cells persist and drive relapse. We found that Dnmt3a mutations induced hematopoietic stem cell expansion, cooperated with mutations in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucleophosmin gene (Npm1(c)) to induce AML in vivo, and promoted resistance to anthracycline chemotherapy. In patients with AML, the presence of DNMT3A(R882) mutations predicts minimal residual disease, underscoring their role in AML chemoresistance. DNMT3A(R882) cells showed impaired nucleosome eviction and chromatin remodeling in response to anthracycline treatment, which resulted from attenuated recruitment of histone chaperone SPT-16 following anthracycline exposure. This defect led to an inability to sense and repair DNA torsional stress, which resulted in increased mutagenesis. Our findings identify a crucial role for DNMT3A(R882) mutations in driving AML chemoresistance and highlight the importance of chromatin remodeling in response to cytotoxic chemotherapy.
Generation of the Fip1l1–Pdgfra fusion gene using CRISPR/Cas genome editing Leukemia 2016 MAR
Abstract
更多信息
| 种属 | Mouse, Other |
|---|---|
| Contains | • IMDM (Iscove's Modified Dulbecco's Medium) • Methylcellulose • Pre-selected serum • Bovine serum albumin • 2-Mercaptoethanol • Phenol red • L-Glutamine • Other ingredients |
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