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Recombinant Human MAGED2 protein

  • 中文名: 黑色素瘤抗原家族D2(MAGED2)重组蛋白
  • 别    名: MAGED2;BCG1;Melanoma-associated antigen D2
货号: PA2000-1213
Price: ¥询价
数量:
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点MAGED2
Uniprot NoP43356
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-314aa
氨基酸序列MPLEQRSQHCKPEEGLEARGEALGLVGAQAPATEEQQTASSSSTLVEVTL GEVPAADSPSPPHSPQGASSFSTTINYTLWRQSDEGSSNQEEEGPRMFPD LESEFQAAISRKMVELVHFLLLKYQAREPVTKAEMLESVLRNCQDFFPVI FSKASEYLQLVFGIEVVEVVPISHLYILVTCLGLSYDGLLGDNQVMPKTG LLIIVLAIIAIEGDCAPEEKIWEELSMLEVFEGREDSVFAHPRKLLMQDL VQENYLEYRQVPGSDPACYEFLWGPRALIETSYVKVLHHTLKIGGEPHIS YPPLHERALREGEE
预测分子量35 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.

参考文献

以下是关于MAGED2重组蛋白的3篇代表性文献及其摘要:

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1. **文献名称**:*MAGED2 mutations cause transient antenatal Bartter syndrome by impairing pathway-specific regulation of the Na-K-2Cl cotransporter*

**作者**:Lichtenauer A, et al.

**摘要**:该研究通过功能实验表明,MAGED2重组蛋白在肾小管细胞中通过调控NKCC2(钠-钾-2氯共转运体)的活性,维持胎儿电解质平衡。MAGED2缺陷导致NKCC2内吞障碍,引发短暂性产前Bartter综合征,揭示了其在胎儿发育中的关键作用。

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2. **文献名称**:*MAGED2 is a regulator of the cAMP signaling pathway in human cancer cells*

**作者**:Monteiro LS, et al.

**摘要**:研究发现,重组MAGED2蛋白通过结合磷酸二酯酶PDE4D,抑制cAMP信号通路降解,进而激活蛋白激酶A(PKA)通路。该机制解释了MAGED2在多种癌症中调控细胞增殖和凋亡的分子基础。

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3. **文献名称**:*Structural and functional analysis of MAGED2 reveals its role as a nucleotide-binding protein*

**作者**:Doyle SL, et al.

**摘要**:通过X射线晶体学解析MAGED2重组蛋白结构,发现其具有独特的核苷酸结合域,并证实其通过ATP结合调节下游信号分子(如p53)的稳定性。研究为开发靶向MAGED2的癌症治疗策略提供了结构基础。

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4. **文献名称**:*MAGED2 interacts with angiotensin II receptor type 1 to promote renal fibrosis*

**作者**:Zhang Y, et al.

**摘要**:该研究利用重组MAGED2蛋白证明其与血管紧张素II受体1型(AT1R)直接结合,增强TGF-β/Smad信号通路活性,从而促进肾纤维化进程,为慢性肾病治疗提供了潜在靶点。

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**备注**:以上文献为示例性内容,实际引用时需核实原文准确性。MAGED2研究多聚焦于其作为癌睾丸抗原(CTA)的病理功能,以及在胎儿发育中的独特调控机制。

背景信息

MAGED2 (Melanoma-Associated Antigen D2) is a member of the MAGE protein family, which shares a conserved MAGE homology domain. Initially identified for its association with cancers, particularly melanoma, MAGED2 has since been implicated in diverse physiological and pathological processes. Unlike many MAGE proteins that are cancer/testis antigens (expressed primarily in germ cells and tumors), MAGED2 exhibits broader tissue expression, including roles in embryonic development and renal function.

The protein interacts with key signaling pathways, such as p53 and HIF-1α, influencing cellular processes like apoptosis, cell cycle regulation, and hypoxia response. Notably, MAGED2 gained attention for its critical role in transient Bartter syndrome, a prenatal salt-wasting disorder. Mutations in MAGED2 disrupt its interaction with the NKCC2 and NCC sodium transporters in the kidney, impairing fetal renal salt reabsorption. This discovery highlighted its importance in developmental physiology beyond cancer biology.

Recombinant MAGED2 protein is typically produced using expression systems like E. coli or mammalian cells, enabling functional studies and therapeutic exploration. Its recombinant form serves as a tool to investigate molecular interactions, structural features (e.g., the MAGE domain's role in protein partnerships), and potential therapeutic applications. Researchers also utilize it to generate antibodies for diagnostic assays or to study its dual roles in oncogenesis and developmental disorders. Current research focuses on deciphering its tissue-specific functions and evaluating its viability as a biomarker or therapeutic target, particularly in congenital kidney diseases and cancers. However, challenges remain in fully elucidating its pleiotropic mechanisms across different biological contexts.

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