| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ARID4B |
| Uniprot No | Q4LE39 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 167-415aa |
| 氨基酸序列 | KQIDELLGKVVCVDYISLDKKKALWFPALVVCPDCSDEIAVKKDNILVRSFKDGKFTSVPRKDVHEITSDTAPKPDAVLKQAFEQALEFHKSRTIPANWKTELKEDSSSSEAEEEEEEEDDEKEKEDNSSEEEEEIEPFPEERENFLQQLYKFMEDRGTPINKRPVLGYRNLNLFKLFRLVHKLGGFDNIESGAVWKQVYQDLGIPVLNSAAGYNVKCAYKKYLYGFEEYCRSANIEFQMALPEKVVNK |
| 预测分子量 | 32.8 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ARID4B重组蛋白的3篇参考文献的简要信息，涵盖其功能、机制及疾病关联研究：
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1. **文献名称**：*ARID4B regulates colorectal cancer stem cell potential through histone demethylase KDM5D-mediated epigenetic modulation*
**作者**：Zhang Y, et al.
**摘要**：该研究揭示了ARID4B通过招募组蛋白去甲基化酶KDM5D调控结直肠癌干性基因的表观遗传修饰，促进肿瘤干细胞自我更新和化疗耐药性。重组ARID4B蛋白的体外实验证实其与KDM5D的直接互作。
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2. **文献名称**：*Structural and functional analysis of the ARID4B-PRC2 complex in epigenetic silencing*
**作者**：Li H, et al.
**摘要**：通过重组ARID4B蛋白与多梳抑制复合物PRC2的体外结合实验，解析了ARID4B通过特定结构域介导PRC2靶向基因启动子，增强H3K27me3修饰并抑制抑癌基因表达的分子机制。
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3. **文献名称**：*ARID4B interacts with p53 to coordinate p21 transcriptional activation in response to DNA damage*
**作者**：Wang X, et al.
**摘要**：研究利用重组ARID4B蛋白及缺失突变体，证明其通过结合p53蛋白增强p21启动子活性，调控细胞周期阻滞。ARID4B缺失导致DNA损伤应答缺陷，提示其在基因组稳定性中的作用。
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*注：上述文献为虚拟示例，实际研究中建议通过PubMed或Web of Science检索具体论文。*
ARID4B (AT-rich interaction domain 4B) is a chromatin-associated protein belonging to the ARID family, characterized by its conserved DNA-binding ARID domain that preferentially interacts with AT-rich genomic regions. It functions as a transcriptional regulator, influencing chromatin remodeling and epigenetic modifications through its association with multi-protein complexes like the SIN3A/HDAC complex, which mediates histone deacacetylation and gene silencing. ARID4B shares structural and functional similarities with its paralog ARID4A, and both are implicated in regulating cell proliferation, differentiation, and apoptosis.
This protein plays critical roles in embryonic development, stem cell maintenance, and tissue homeostasis. Dysregulation of ARID4B has been linked to cancer, where it may act as either an oncogene or tumor suppressor depending on context. For instance, ARID4B overexpression is observed in prostate and breast cancers, promoting tumor growth by repressing tumor suppressor genes. Conversely, its loss has been associated with genomic instability in certain malignancies.
Recombinant ARID4B proteins are engineered for functional studies, typically expressed in bacterial or mammalian systems with affinity tags (e.g., His-tag, GST) for purification. These tools enable researchers to investigate ARID4B's DNA-binding specificity, protein-protein interactions, and enzymatic activities in vitro. Recent studies employ recombinant ARID4B to screen small-molecule inhibitors targeting its oncogenic functions or to map post-translational modifications regulating its activity. Its dual role in cancer pathways makes it a compelling subject for therapeutic exploration and mechanistic studies of epigenetic regulation.
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