OGS589
PBR322 - PBR322 低拷贝克隆载体
plasmid vector for molecular cloning
同義詞:
snapfast 载体
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| 包裝尺寸 | 庫存單位 | 供貨能力 | 價格 |
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關於此項目
NACRES:
NA.85
UNSPSC Code:
12352200
Origin of replication:
BR322 (15 copies)
Bacteria selection:
ampicillin
Reporter gene:
none
Peptide cleavage:
no cleavage
暫時無法取得訂價和供貨情況
form
buffered aqueous solution
mol wt
size 4361 bp
bacteria selection
ampicillin
origin of replication
BR322 (15 copies)
peptide cleavage
no cleavage
reporter gene
none
shipped in
ambient
storage temp.
−20°C
General description
该质粒含有 BR322（低拷贝数）复制起点，并为每个细菌细胞提供约 20 个质粒拷贝。它还包含用于选择转染哺乳动物细胞的MCS和Kan 抗性的哺乳动物CMV启动子上游。低拷贝数质粒对非常大的转基因或对细菌细胞有毒性的转基因是有用的。
启动子表达水平：
启动子表达水平：
Application
BR322 信息： BR322 是从大肠杆菌中分离得到的野生型质粒。其含有低拷贝来源，允许质粒以每个细胞约 10-100 个质粒拷贝的频率维持。通常每个细胞的这一数字接近 30-40个拷贝。最常见的克隆质粒含有该质粒中称为pUC的复制起点的衍生物。pUC 的起源是通过去除 Rep 阻遏蛋白形成的。阻遏蛋白通常在大肠杆菌中调节质粒拷贝数，也在复制起始点本身进行单点突变。点突变是复制起点之间最重要的差异。该质粒可作为通用低拷贝克隆载体。
Analysis Note
欲查看本品的分析证书，请访问 www.oxgene.com
Other Notes
欲查看本品的序列信息，请访问 产品页面。
存儲類別/等級
12 - Non Combustible Liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
Diana Romero et al.
Carcinogenesis, 37(1), 18-29 (2015-10-28)
Dickkopf-3 (Dkk-3) is a secreted protein whose expression is downregulated in many types of cancer. Endogenous Dkk-3 is required for formation of acini in 3D cultures of prostate epithelial cells, where it inhibits transforming growth factor (TGF)-β/Smad signaling. Here, we
Geoffrey M Lynn et al.
Nature biotechnology, 33(11), 1201-1210 (2015-10-27)
The efficacy of vaccine adjuvants such as Toll-like receptor agonists (TLRa) can be improved through formulation and delivery approaches. Here, we attached small molecule TLR-7/8a to polymer scaffolds (polymer-TLR-7/8a) and evaluated how different physicochemical properties of the TLR-7/8a and polymer
Jin-Gyoung Jung et al.
PLoS genetics, 10(10), e1004751-e1004751 (2014-10-31)
The Notch3 signaling pathway is thought to play a critical role in cancer development, as evidenced by the Notch3 amplification and rearrangement observed in human cancers. However, the molecular mechanism by which Notch3 signaling contributes to tumorigenesis is largely unknown.