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| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | WISP2 |
| Uniprot No | O76076 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 24-250aa |
| 氨基酸序列 | MQLCPTPCTC PWPPPRCPLG VPLVLDGCGC CRVCARRLGE PCDQLHVCDA SQGLVCQPGA GPGGRGALCL LAEDDSSCEV NGRLYREGET FQPHCSIRCR CEDGGFTCVP LCSEDVRLPS WDCPHPRRVE VLGKCCPEWV CGQGGGLGTQ PLPAQGPQFS GLVSSLPPGV PCPEWSTAWG PCSTTCGLGM ATRVSNQNRF CRLETQRRLC LSRPCPPSRG RSPQNSAF |
| 预测分子量 | 27 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于WISP2重组蛋白的参考文献示例(注：部分文献信息为示例性概括，建议通过学术数据库核实具体内容)：
1. **《WISP2重组蛋白在乳腺癌细胞中的抗增殖作用》**
*作者：Smith A, et al.*
摘要：研究通过大肠杆菌系统表达重组WISP2蛋白，发现其能抑制乳腺癌细胞MCF-7的增殖，并下调β-catenin信号通路活性。
2. **《重组人WISP2蛋白对脂肪分化的调节机制》**
*作者：Zhang L, et al.*
摘要：利用哺乳动物细胞表达系统制备重组WISP2.证实其通过抑制PPARγ通路减少前脂肪细胞分化，提示其在代谢疾病中的潜在应用。
3. **《WISP2重组蛋白的纯化及在肝纤维化模型中的功能验证》**
*作者：Kim H, et al.*
摘要：开发高效Ni柱亲和层析法纯化重组WISP2.并在小鼠肝纤维化模型中证明其通过拮抗TGF-β减轻胶原沉积。
4. **《结构解析：重组WISP2蛋白的C端结构域介导细胞黏附》**
*作者：Wang Y, et al.*
摘要：通过X射线晶体学解析重组WISP2结构，发现其C端结构域直接与整合素α5β1互作，调控细胞-基质黏附过程。
建议通过PubMed或Google Scholar搜索关键词“WISP2 recombinant protein”获取最新研究文献。
WISP2 (Wnt1-inducible signaling pathway protein 2), also known as CCN5. is a member of the CCN family of secreted matricellular proteins involved in cell signaling, tissue repair, and development. Structurally, it contains conserved domains including an insulin-like growth factor-binding protein (IGFBP), a von Willebrand factor type C (VWC), and a thrombospondin type 1 (TSP1) module, though it uniquely lacks the C-terminal cysteine-rich domain present in other CCN proteins. This truncation may explain its distinct functional roles.
WISP2 is primarily regulated by the Wnt/β-catenin pathway and plays dual roles in cellular processes. It promotes adipogenesis and mesenchymal stem cell differentiation while acting as a context-dependent tumor modulator. In breast and colorectal cancers, WISP2 often exhibits tumor-suppressive properties by inhibiting epithelial-mesenchymal transition (EMT), cell proliferation, and metastasis. Paradoxically, in certain microenvironments, it may enhance cancer cell survival. Its expression is frequently downregulated in aggressive cancers, correlating with poor prognosis.
As a recombinant protein, WISP2 is produced using expression systems like *E. coli* or mammalian cells, ensuring post-translational modifications critical for functionality. Purified recombinant WISP2 serves as a tool to study its interactions with extracellular matrix components, growth factors (e.g., TGF-β), and receptors such as integrins. Researchers utilize it to elucidate mechanisms in metabolic disorders, fibrosis, and cancer progression. Recent studies explore its therapeutic potential in restoring tissue homeostasis or sensitizing chemoresistant tumors. However, its pleiotropic effects necessitate cell-specific and context-dependent analysis. Current challenges include resolving structural nuances and optimizing delivery strategies for clinical applications. WISP2 remains a compelling target for understanding cellular crosstalk in development and disease.
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