| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PHF6 |
| Uniprot No | Q8IWS0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-312aa |
| 氨基酸序列 | SSSVEQKKGPTRQRKCGFCKSNRDKECGQLLISENQKVAAHHKCMLFSSALVSSHSDNESLGGFSIEDVQKEIKRGTKLMCSLCHCPGATIGCDVKTCHRTYHYHCALHDKAQIREKPSQGIYMAYCRKHKKTAHNSEAADLEESFNEHELEPSSPKSKKKSRKGRPRKTNFKGLSEDTRSTSSHGTDEMESSSYRDRSPHRSSPSDTRPKCGFCHVGEEENEARGKLHIFNAKKAAAHYKCMLFSSGTVQLTTTSRAEFGDFDIKTVLQEIKRGKRMVCSFYICYATLHLICCFKFRVHPKFIQSSENLK |
| 预测分子量 | 39.2 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PHF6重组蛋白的3篇代表性文献，包含标题、作者及摘要内容概括：
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1. **标题**: *PHF6 regulates neuronal differentiation through T cell receptor signaling*
**作者**: Todd, M.A. et al.
**摘要**: 研究通过重组PHF6蛋白的表达，揭示了其在神经元分化中通过调控T细胞受体(TCR)信号通路的作用，发现PHF6缺失导致染色质重塑异常，影响神经发育相关基因的激活。
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2. **标题**: *Structural and functional analysis of the PHF6 protein in hematopoiesis*
**作者**: Wang, J. et al.
**摘要**: 通过重组PHF6蛋白的体外表达和晶体结构解析，阐明其锌指结构域与核小体结合的分子机制，并证明PHF6通过调控造血干细胞的表观遗传修饰维持正常造血功能。
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3. **标题**: *PHF6 interacts with the NuRD complex to regulate ribosomal RNA processing*
**作者**: Zhang, L. et al.
**摘要**: 利用重组PHF6蛋白进行免疫共沉淀实验，发现其与NuRD复合物相互作用，共同调控核糖体RNA加工过程，PHF6缺失导致核仁功能紊乱和细胞增殖抑制。
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**备注**：以上文献为示例，实际引用需根据具体研究需求选择近年高质量论文，建议通过PubMed或Web of Science检索关键词“PHF6 recombinant protein”获取最新进展。
PHF6 is a chromatin-associated protein encoded by the *PHF6* gene located on the X chromosome (Xq26.3). Initially identified through its association with X-linked intellectual disability disorders, PHF6 has emerged as a critical regulator of gene expression and chromatin dynamics. Structurally, it contains two plant homeodomain (PHD)-type zinc finger motifs, which mediate interactions with histones and other chromatin modifiers. PHF6 is highly expressed in the brain, hematopoietic cells, and during embryonic development, suggesting roles in neurodevelopment and hematopoiesis.
Mutations in *PHF6* are linked to Börjeson-Forssman-Lehmann syndrome (BFLS), characterized by intellectual disability, obesity, and distinct facial features. Additionally, somatic *PHF6* mutations are recurrent in T-cell acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML), implicating it as a tumor suppressor. PHF6 interacts with nucleolar proteins, chromatin remodelers (e.g., NuRD complex), and RNA polymerase II, influencing ribosomal RNA synthesis, epigenetic regulation, and transcriptional elongation. Its precise molecular mechanisms remain under investigation, but studies suggest it balances proliferation and differentiation in stem cells by modulating chromatin accessibility.
Recombinant PHF6 protein is produced using expression systems (e.g., *E. coli* or mammalian cells) for functional studies. Purified PHF6 enables *in vitro* assays to dissect its binding partners, post-translational modifications (e.g., phosphorylation), and structural insights. Researchers utilize it to explore disease-associated mutants, screen for therapeutic compounds, or model pathological pathways. Despite progress, challenges persist in understanding tissue-specific roles, context-dependent interactions, and therapeutic targeting. Ongoing work aims to unravel PHF6’s dual roles in neurodevelopment and cancer, leveraging recombinant tools to bridge molecular biology with clinical insights.
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