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进一步了解 >> 我们的质量体系通过ISO 9001认证。这些产品是在我们先进的设施中严格控制下生成的。

质粒DNA制备

高质量质粒DNA对于众多分子生物学实验非常重要，例如载体克隆、细胞转染、病毒包装、重组蛋白制备等。云舟生物提供从ug到g级别的快速、经济、可定制的质粒DNA制备服务，可满足从基础科研到工业应用的多样化需求。除科研级、科研级Plus和工业级质粒外，我们也提供符合GMP标准的大规模质粒DNA制备服务。

如果您对质粒的安全性、可制造性、效用等方面有很高的要求，请查看我们专有的无需抗生素和无需添加剂的miniVec® 载体系统。

亮点
Research Grade科研级
  • 适用于载体克隆等多种基础分子生物学实验
  • 周期短、性价比高
Research Plus Grade科研级Plus
  • 适用于细胞转染、病毒包装、重组蛋白表达、体内实验等应用
  • 产量范围100 ug到10 mg
  • 高超螺旋比例（80±10%）、低内毒素水平（<0.05 EU/ug）
Industrial Grade工业级
  • 适用于临床前应用以及大规模下游生产
  • 可高度自定义的产量（100 ug到1 g）和QC项目
  • 更高的超螺旋比例（85±10%）、更低的内毒素水平（<0.01 EU/ug）
  • 支持无动物源生产
服务详情
价格与周期
等级规格产量价格(CNY)周期应用
科研级质粒⼩提高拷贝：>10 ug（>200 ng/ul，50 ul）￥1801-2天载体克隆等基础分子生物学实验
中、低拷贝：>5 ug（>100 ng/ul，50 ul）
科研级Plus质粒中提高拷贝：>100 ug（>1 ug/ul，100 ul）￥5802-4天多种细胞实验（如转染、病毒包装、重组蛋白表达、体外试验等）、体内实验
中、低拷贝：>50 ug（>500 ng/ul，100 ul）
质粒⼤提高拷贝：>300 ug（>1 ug/ul，300 ul）￥880
中、低拷贝：>150 ug（>500 ng/ul，300 ul）
质粒超⼤提高拷贝：>1 mg（>1 ug/ul，1 ml）￥1,480
中、低拷贝：>0.5 mg（>500 ng/ul，1 ml）
质粒特大提高拷贝：>10 mg（>1 ug/ul，10 ml）￥5,3805-7天
中、低拷贝：>5 mg（>500 ng/ul，10 ml）
工业级100 ug ~ 1 g请咨询临床前实验（如效用和安全性研究）、用于工业应用的重组蛋白、病毒、IVT RNA的大规模生产

注：以上报价不适用治疗性IVT RNA的IVT质粒载体制备。该类IVT质粒载体对比常规科研等级的质粒载体在纯度、超螺旋比例等参数上的标准更特殊。

无动物源质粒生产

云舟生物可提供不含TSE/BSE的无动物源质粒制备服务。我们可使用植物源培养基生产质粒DNA，并且纯化过程可经过无酶处理。根据您的需求，我们可提供相应的TSE/BSE声明。

运输和存储

我们的质粒DNA默认存储于1xTE缓冲液，以常温方式运输。质粒DNA可以在4°C短期保存2周。如果您需要长期存储，请将质粒DNA放置于-20°C or -80°C保存。避免反复冻融。

客户提供材料

如需客户提供载体，则请按照外来物品接收指南将载体寄送给我们。请严格按照我们的指南来进行装运以免造成物品的任何延误和损坏。客户提供的所有材料均需经过QC检测，每一份材料附加检测费用。请注意，客户提供物品接收并通过QC之后生产才正式开始。周期是指订单接收到发货之间的时间，不包括需要客户提供任何物料（如客户提供载体）的等待时间以及所需的QC时间。

技术详情
质量控制
属性QC方法科研级科研级Plus工业级
一般特性外观目视检测✓✓✓
浓度Nanodrop✓✓✓
质粒鉴定质粒大小酶切分析✓✓✓
插入片段Sanger测序选购选购选购
质粒全长序列Sanger测序选购选购选购
NGS选购选购选购
纯度OD260/280Nanodrop✓✓✓
超螺旋比例琼脂糖凝胶电泳N/A✓
80 ± 10%		✓
≥85%
残留蛋白BCAN/AN/A选购
残留E. coli RNA琼脂糖凝胶上不可见N/A✓✓
荧光测定法N/AN/A选购
残留E. coli DNA琼脂糖凝胶上不可见N/A✓✓
qPCRN/AN/A选购
安全性无菌性直接接种N/A✓✓
内毒素水平鲎试剂动态显色法N/A✓
<0.05 EU/ug		✓
<0.01 EU/ug
噬菌体检测PCRN/A只适用于质粒特大提✓ （规格需要>10 mg）
文件--COA（根据需求）COA（根据需求）
1. COA
2. TSE/BSE声明（根据需求）
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Lactic acid promotes PD-1 expression in regulatory T cells in highly glycolytic tumor microenvironments
Lactic acid promotes PD-1 expression in regulatory T cells in highly glycolytic tumor microenvironments
Cancer Cell, 2022, doi: 10.1016/j.ccell.2022.01.001
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Abstract: The balance of programmed death-1 (PD-1)-expressing CD8+ T cells and regulatory T (Treg) cells in the tumor microenvironment (TME) determines the clinical efficacy of PD-1 blockade therapy through the competition of their reactivation. However, factors that determine this balance remain unknown. Here, we show that Treg cells gain higher PD-1 expression than effector T cells in highly glycolytic tumors, including MYC-amplified tumors and liver tumors. Under low-glucose environments via glucose consumption by tumor cells, Treg cells actively absorbed lactic acid (LA) through monocarboxylate transporter 1 (MCT1), promoting NFAT1 translocation into the nucleus, thereby enhancing the expression of PD-1, whereas PD-1 expression by effector T cells was dampened. PD-1 blockade invigorated the PD-1-expressing Treg cells, resulting in treatment failure. We propose that LA in the highly glycolytic TME is an active checkpoint for the function of Treg cells in the TME via upregulation of PD-1 expression.
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Glycine decarboxylase maintains mitochondrial protein lipoylation to support tumor growth
Glycine decarboxylase maintains mitochondrial protein lipoylation to support tumor growth
Dzmitry Mukha, et al.
Cell Metabolism, 2022, doi: 10.1016/j.cmet.2022.04.006
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Abstract: The folic acid cycle mediates the transfer of one-carbon (1C) units to support nucleotide biosynthesis. While the importance of serine as a mitochondrial and cytosolic donor of folate-mediated 1C units in cancer cells has been thoroughly investigated, a potential role of glycine oxidation remains unclear. We developed an approach for quantifying mitochondrial glycine cleavage system (GCS) flux by combining stable and radioactive isotope tracing with computational flux decomposition. We find high GCS flux in hepatocellular carcinoma (HCC), supporting nucleotide biosynthesis. Surprisingly, other than supplying 1C units, we found that GCS is important for maintaining protein lipoylation and mitochondrial activity. Genetic silencing of glycine decarboxylase inhibits the lipoylation and activity of pyruvate dehydrogenase and impairs tumor growth, suggesting a novel drug target for HCC. Considering the physiological role of liver glycine cleavage, our results support the notion that tissue of origin plays an important role in tumor-specific metabolic rewiring.
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Dominant mutations in MIEF1 affect mitochondrial dynamics and cause a singular late onset optic neuropathy
Dominant mutations in MIEF1 affect mitochondrial dynamics and cause a singular late onset optic neuropathy
Majida Charif, et al.
Molecular Neurodegeneration, 2021, doi: 10.1186/s13024-021-00431-w
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Abstract: Inherited optic neuropathies are the most common mitochondrial diseases, leading to neurodegeneration involving the irreversible loss of retinal ganglion cells, optic nerve degeneration and central visual loss. Importantly, properly regulated mitochondrial dynamics are critical for maintaining cellular homeostasis, and are further regulated by MIEF1 (mitochondrial elongation factor 1) which encodes for MID51 (mitochondrial dynamics protein 51), an outer mitochondrial membrane protein that acts as an adaptor protein to regulate mitochondrial fission. However, dominant mutations in MIEF1 have not been previously linked to any human disease. Using targeted sequencing of genes involved in mitochondrial dynamics, we report the first heterozygous variants in MIEF1 linked to disease, which cause an unusual form of late-onset progressive optic neuropathy characterized by the initial loss of peripheral visual fields. Pathogenic MIEF1 variants linked to optic neuropathy do not disrupt MID51's localization to the outer mitochondrial membrane or its oligomerization, but rather, significantly disrupt mitochondrial network dynamics compared to wild-type MID51 in high spatial and temporal resolution confocal microscopy live imaging studies. Together, our study identifies dominant MIEF1 mutations as a cause for optic neuropathy and further highlights the important role of properly regulated mitochondrial dynamics in neurodegeneration.
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