| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | Ccn5 |
| Uniprot No | O76076 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-250aa |
| 氨基酸序列 | MRGTPKTHLLAFSLLCLLSKVRTQLCPTPCTCPWPPPRCPLGVPLVLDGCGCCRVCARRLGEPCDQLHVCDASQGLVCQPGAGPGGRGALCLLAEDDSSCEVNGRLYREGETFQPHCSIRCRCEDGGFTCVPLCSEDVRLPSWDCPHPRRVEVLGKCCPEWVCGQGGGLGTQPLPAQGPQFSGLVSSLPPGVPCPEWSTAWGPCSTTCGLGMATRVSNQNRFCRLETQRRLCLSRPCPPSRGRSPQNSAF |
| 预测分子量 | 36.6 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3篇关于CCN5(WISP2)重组蛋白研究的文献概览，内容涵盖其功能机制及疾病相关性：
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1. **文献名称**：*CCN5 suppresses hepatocellular carcinoma via inhibition of epithelial-mesenchymal transition and Wnt/β-catenin signaling*
**作者**：Zhang Y, et al.
**摘要**：研究利用重组CCN5蛋白处理肝癌细胞，发现其通过抑制Wnt/β-catenin通路和EMT过程，显著降低肝癌细胞侵袭转移能力，并延缓小鼠模型中肿瘤生长。
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2. **文献名称**：*Recombinant CCN5 protein inhibits breast cancer progression through modulation of ERα signaling*
**作者**：Berschneider B, et al.
**摘要**：通过大肠杆菌表达系统制备重组CCN5.实验证明其与雌激素受体α(ERα)互作，抑制乳腺癌细胞增殖并诱导凋亡，提示其在ER阳性乳腺癌治疗中的潜在价值。
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3. **文献名称**：*CCN5 attenuates profibrotic phenotypes of fibroblasts through blocking TGF-β/Smad signaling*
**作者**：Jun JI, Lau LF
**摘要**：利用哺乳动物细胞表达的重组CCN5蛋白，发现其可通过竞争性结合TGF-β受体，抑制成纤维细胞向肌成纤维细胞转化，为抗纤维化治疗提供新策略。
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**备注**：以上文献为示例性内容，实际文献需通过PubMed/Google Scholar以"CCN5/WISP2 recombinant protein"等关键词检索获取。部分早期关键研究可能发表于《Journal of Cell Communication and Signaling》等CCN家族专刊。
**Background of Recombinant CCN5 Protein**
CCN5. also known as WISP2 (Wnt1-inducible signaling pathway protein 2), is a member of the CCN family of matricellular proteins, which includes six conserved cysteine-rich secreted proteins (CCN1–6). These proteins play critical roles in regulating cell proliferation, differentiation, adhesion, migration, and extracellular matrix (ECM) remodeling. Unlike other CCN members, CCN5 lacks the C-terminal (CT) domain, which influences its functional interactions with growth factors, cytokines, and ECM components. This structural distinction may underlie its unique role in modulating cellular processes, particularly in fibrotic diseases, cancer, and tissue repair.
Recombinant CCN5 protein is produced using genetic engineering techniques, typically expressed in bacterial, mammalian, or insect cell systems to ensure proper post-translational modifications. Its production enables detailed studies of its molecular mechanisms and therapeutic potential. CCN5 has garnered attention for its dual roles in disease contexts. In fibrosis, it acts as an antifibrotic factor by inhibiting TGF-β/Smad signaling and ECM deposition. In cancer, CCN5 exhibits context-dependent behavior—it suppresses tumor progression in certain cancers (e.g., breast and pancreatic) by blocking epithelial-mesenchymal transition (EMT) and metastasis, yet may promote tumorigenesis in others.
Research on recombinant CCN5 has expanded into exploring its therapeutic applications. Preclinical studies highlight its potential in attenuating fibrosis in cardiac, renal, and pulmonary tissues, as well as its ability to enhance wound healing. Additionally, its role in metabolic disorders, such as obesity and diabetes, is emerging. Despite progress, challenges remain in understanding its signaling networks and optimizing delivery systems for clinical use. Overall, recombinant CCN5 serves as a valuable tool for unraveling disease mechanisms and developing targeted therapies.
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