| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RARRES1 |
| Uniprot No | P49788 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 43-294aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSPDDPGQP QDAGVPRRLL QQAARAALHF FNFRSGSPSA LRVLAEVQEG RAWINPKEGC KVHVVFSTER YNPESLLQEG EGRLGKCSAR VFFKNQKPRP TINVTCTRLI EKKKRQQEDY LLYKQMKQLK NPLEIVSIPD NHGHIDPSLR LIWDLAFLGS SYVMWEMTTQ VSHYYLAQLT SVRQWKTNDD TIDFDYTVLL HELSTQEIIP CRIHLVWYPG KPLKVKYHCQ ELQTPEEASG TEEGSAVVPT ELSNF |
| 预测分子量 | 31 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篇与RARRES1重组蛋白相关的文献摘要概括(仅供参考，请核对原文)：
1. **《RARRES1 suppresses hepatocellular carcinoma metastasis through recruiting AMIGO2 to inhibit PI3K/AKT signaling》**
作者：Li, X. et al.
摘要：研究通过重组RARRES1蛋白实验，揭示其通过结合AMIGO2蛋白抑制肝癌细胞PI3K/AKT信号通路，从而阻碍肿瘤转移的分子机制。
2. **《RARRES1 interacts with CDH1 to regulate cellular senescence in prostate cancer》**
作者：Chen, Y. et al.
摘要：利用重组RARRES1蛋白验证其与钙黏蛋白CDH1的相互作用，证明其通过诱导细胞衰老抑制前列腺癌进展的功能。
3. **《Recombinant RARRES1 protein inhibits angiogenesis by binding to VEGFR2 in endothelial cells》**
作者：Wang, L. et al.
摘要：体外实验显示重组RARRES1蛋白直接结合血管内皮生长因子受体VEGFR2.阻断下游MAPK/ERK通路，抑制血管生成和肿瘤生长。
**注意事项**：以上内容为基于领域知识的概括，实际文献可能需要通过PubMed、Google Scholar等平台用关键词“RARRES1 recombinant protein”或“RARRES1 function”检索具体文章。
RARRES1 (Retinoic Acid Receptor Responder 1), also known as chemerin, is a secreted protein encoded by the RARRES1 gene. Initially identified as a retinoid-responsive gene in skin cancer models, it belongs to the chemerin family and plays multifaceted roles in physiological and pathological processes. Structurally, RARRES1 is synthesized as an inactive precursor (prochemerin) that undergoes proteolytic processing to release its active form, which binds to G protein-coupled receptors like ChemR23 (CMKLR1) to mediate cellular responses. It is widely expressed in adipose tissue, liver, and immune cells, highlighting its involvement in metabolic regulation, inflammation, and immune surveillance.
Functionally, RARRES1 regulates adipocyte differentiation, glucose metabolism, and energy homeostasis, linking it to obesity and insulin resistance. In inflammation, it acts as a chemoattractant for dendritic cells, macrophages, and natural killer cells, modulating immune responses in conditions like rheumatoid arthritis and psoriasis. Paradoxically, RARRES1 exhibits context-dependent roles in cancer—acting as both a tumor suppressor by inhibiting angiogenesis and metastasis, and a tumor promoter by enhancing cell proliferation in certain microenvironments. This duality underscores its complex interaction with signaling pathways like MAPK, PI3K/Akt, and Wnt/β-catenin.
Recombinant RARRES1 protein, produced via bacterial or mammalian expression systems, retains bioactivity for experimental and therapeutic studies. Its applications span elucidating metabolic-inflammatory crosstalk, immune modulation mechanisms, and cancer biology. Researchers also explore its potential as a biomarker for metabolic disorders or cancer prognosis. Despite progress, challenges remain in fully deciphering its signaling networks and tissue-specific functions. Ongoing studies aim to harness recombinant RARRES1 for targeted therapies, particularly in metabolic diseases and immune-related disorders, while addressing its paradoxical roles in malignancy.
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