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- Purity>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
- Endotoxin Level<0.10 eu="" per="" 1="" μg="" of="" the="" protein="" by="" the="" lal="">0.10>
- Activity
- SourceSpodoptera frugiperda, Sf 21 (baculovirus)-derived Ser26-Ile259, with Leu35Pro substitution and a C-terminal 10-His tag
- Accession #
- N-terminal Sequence
AnalysisSer26 - Predicted Molecular Mass27 kDa
- SDS-PAGE29-35 kDa, reducing conditions
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- Long Name:Dickkopf-2
- Entrez Gene IDs:27123 (Human); 56811 (Mouse)
- Alternate Names:dickkopf (Xenopus laevis) homolog 2; dickkopf 2; dickkopf homolog 2 (Xenopus laevis); dickkopf related protein-2; dickkopf-2; dickkopf-related protein 2; Dkk2; Dkk-2; hDkk-2
Background:
Dickkopf related protein 2 (Dkk-2) is a member of the Dickkopf family of secreted Wnt modulators (1-3). Dkk proteins contain a signal peptide and two conserved cysteine-rich domains that are separated by a linker region. The second cysteine-rich domain mediates Dkk-2 binding activities, and its interaction with LRP beta propellers has been mapped (2-4, 7). The 226 aa, ~35 kDa mature mouse Dkk-2 shares 99%, 96%, 96%, 96% and 94% aa identity with rat, human, dog, horse and cow Dkk-2, respectively, and can activate the canonical Wnt signaling pathway in Xenopus embryos (5). Dkk proteins modify Wnt engagement of a receptor complex composed of a Frizzled protein and a low-density lipoprotein receptor-related protein, either LRP5 or LRP6 (3). When LRP6 is over-expressed, direct high-affinity binding of Dkk-2 to LRP can enhance canonical Wnt signaling (6-8). However, when Dkk-2 and LRP6 form a ternary complex with Kremen2, Wnt signaling is inhibited due to internalization of Dkk-2/LRP6/Krm2 complexes (9, 10). Thus, depending on the cellular context, Dkk-2 can either activate or inhibit canonical Wnt signaling (3). In contrast, binding of Dkk-1 or Dkk-4 to LRP is consistently antagonistic (3). Dkk proteins are expressed in mesenchymal tissues and control epithelial transformations. Dkk-2 expression has been studied most in bone and eye, although it is expressed as early as periimplantation in mice (11). Mouse Dkk-1 or Dkk-2 deficiencies have opposite effects on bone homeostasis, despite down-regulating Wnt antagonism in both cases (12, 13). Dkk-2 expression is induced by Wnts in bone, and is thought to enhance bone density by promoting terminal differentiation of osteoblasts and mineral deposition (12). In contrast, Dkk-1 negatively regulates late osteoblast proliferation, which limits bone density (13). Dkk-2-deficient mice are blind, exhibiting faulty differentiation of corneal epithelium and ectopic blood vessels in the periocular mesenchyme (14, 15).
R&D Systems位于美国的明尼苏达州,一直致力于生物制品的开发与生产。公司成立之初主要生产用于医院及临床应用的血控品。1997年,公司推出第一个产品--富血小板血浆质控品;1981年,公司成为全球第二家生产含血小板全血控品的供应商。40多年的发展中,R&D Systems仍持续开发各种血控品产品。 1985年,作为公司推出的第一个科研试剂产品,也是全球第一家将该产品进行商业化生产的产品,R&D Systems成功上市了TGF-beta1蛋白。作为胞外信号分子,TGF-beta1蛋白在多种细胞中进行表达,并作为胞外信号分子参与免疫功能,细胞增殖和细胞分化等生物学过程。该产品推出后,公司陆续从生物材料中纯化了几种细胞因子产品并推向市场。 天然蛋白类产品的成功推广,加速了R&D Systems在细胞因子市场的开拓。公司于1985年形成Growth Factor事业部(现Biotechnology事业部)。Biotechnology事业部的目标是生产和营销重组人细胞因子。与天然来源提取蛋白相比较,DNA重组技术生产的蛋白产品其成本更低,产量更高,完全摆脱原料的限制。1989年,Biotechnology事业部开始开发抗细胞因子的单克隆和多克隆抗体,并于1990年开发了第一个ELISA试剂盒。 2014年2月10日,R&D Systems的母公司宣布命名为Bio-Techne. Bio-Techne旗下包括R&D Systems, Novus Biologicals, BiosPacific, Tocris Bioscience, Boston Biochem和Bionostics。

