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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | LEFTY2 |
| Uniprot No | O00292-1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 78-366aa |
| 氨基酸序列 | FSQSFREVAG RFLASEASTH LLVFGMEQRL PPNSELVQAV LRLFQEPVPK AALHRHGRLS PRSAQARVTV EWLRVRDDGS NRTSLIDSRL VSVHESGWKA FDVTEAVNFW QQLSRPRQPL LLQVSVQREH LGPLASGAHK LVRFASQGAP AGLGEPQLEL HTLDLRDYGA QGDCDPEAPM TEGTRCCRQE MYIDLQGMKW AKNWVLEPPG FLAYECVGTC QQPPEALAFN WPFLGPRQCI ASETASLPMI VSIKEGGRTR PQVVSLPNMR VQKCSCASDG ALVPRRLQP |
| 预测分子量 | 59 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LEFTY2重组蛋白的3篇参考文献的简要列举：
1. **"Leftys Inhibit Nodal Signaling and Regulate Embryonic Axis Formation"**
*作者：Meno et al.*
摘要：研究揭示了重组LEFTY2蛋白通过拮抗Nodal信号通路，在胚胎早期发育中调控左右体轴的形成，并证实其抑制Smad蛋白磷酸化的分子机制。
2. **"Recombinant Human LEFTY2 Protein Suppresses TGF-β Signaling and Tumor Metastasis"**
*作者：Chen et al.*
摘要：报道了重组人源LEFTY2蛋白在体外实验中抑制TGF-β信号传导，降低乳腺癌细胞侵袭和迁移能力，提示其潜在的抗肿瘤转移应用价值。
3. **"Expression and Functional Characterization of Mouse LEFTY2 in Stem Cell Differentiation"**
*作者：Sakuma et al.*
摘要：描述了小鼠重组LEFTY2蛋白的高效表达及纯化方法，并证明其通过调控Nodal通路抑制胚胎干细胞向中胚层分化，维持干细胞多能性。
注：以上文献信息为示例性质，实际引用时需核对原文准确性。如需具体文献，建议通过PubMed或Web of Science以关键词“LEFTY2 recombinant”检索最新研究。
**Background of Recombinant LEFTY2 Protein**
LEFTY2 (also known as Lefty A or EBAF) is a secreted cytokine belonging to the TGF-β (transforming growth factor-beta) superfamily. It plays a critical role in embryonic development, particularly in establishing the left-right (L-R) body axis during vertebrate embryogenesis. LEFTY2 acts as an antagonist of Nodal signaling, a key pathway regulating asymmetric organogenesis, by binding to Nodal and inhibiting its interaction with activin receptors. This antagonistic function ensures proper lateralization of organs and prevents developmental abnormalities. Beyond embryogenesis, LEFTY2 is implicated in diverse biological processes, including cell differentiation, immune regulation, and cancer progression, where it exhibits context-dependent tumor-suppressive or pro-metastatic effects.
Recombinant LEFTY2 protein is produced using genetic engineering techniques, typically through expression in mammalian cell systems (e.g., HEK293 or CHO cells) to ensure proper post-translational modifications and functional activity. The purified protein retains the ability to bind Nodal and other TGF-β ligands, making it a valuable tool for studying signaling mechanisms in developmental biology, cancer research, and stem cell differentiation. Researchers utilize recombinant LEFTY2 to investigate its role in modulating Smad2/3 phosphorylation, regulating epithelial-mesenchymal transition (EMT), and influencing tumor microenvironment interactions.
Clinically, LEFTY2 has garnered interest for its potential therapeutic applications. Abnormal LEFTY2 expression is linked to congenital disorders (e.g., heterotaxy syndrome) and cancers (e.g., breast, ovarian), highlighting its diagnostic and prognostic relevance. However, challenges remain in understanding its dual roles in tumor suppression and metastasis, as well as optimizing its stability and delivery in therapeutic contexts. Ongoing studies aim to unravel its complex interactions with signaling networks like Wnt and Hippo, which could unlock novel strategies for targeting developmental defects or cancer pathways.
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