| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TLX3 |
| Uniprot No | O43711 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-291 aa |
| 活性数据 | MEAPASAQTP HPHEPISFGI DQILNSPDQD SAPAPRGPDG ASYLGGPPGG RPGATYPSLP ASFAGLGAPF EDAGSYSVNL SLAPAGVIRV PAHRPLPGAV PPPLPSALPA MPSVPTVSSL GGLNFPWMES SRRFVKDRFT AAAALTPFTV TRRIGHPYQN RTPPKRKKPR TSFSRVQICE LEKRFHRQKY LASAERAALA KSLKMTDAQV KTWFQNRRTK WRRQTAEERE AERQQASRLM LQLQHDAFQK SLNDSIQPDP LCLHNSSLFA LQNLQPWEED SSKVPAVTSL V |
| 分子量 | 31.8 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. |
以下是关于重组人TLX3蛋白的3篇参考文献示例(文献标题和摘要为模拟内容，供参考)：
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1. **文献名称**: *TLX3-induced transcriptional deregulation in T-cell acute lymphoblastic leukemia*
**作者**: Smith A et al.
**摘要**: 研究揭示了TLX3蛋白在T-ALL中的致癌机制，通过重组TLX3蛋白实验证明其异常表达破坏造血分化关键基因(如NOTCH1)的调控，导致细胞增殖失控。
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2. **文献名称**: *Structural basis of TLX3-DNA interaction and its role in oncogenesis*
**作者**: Li X et al.
**摘要**: 通过X射线晶体学解析重组TLX3蛋白的DNA结合域结构，阐明其特异性识别靶基因启动子区域的分子机制，为靶向药物设计提供依据。
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3. **文献名称**: *TLX3 reprograms cell metabolism by regulating mitochondrial genes in leukemia*
**作者**: Wang Y et al.
**摘要**: 利用重组TLX3蛋白的体外模型，证实其通过激活糖酵解相关基因(如HK2)，驱动白血病细胞的代谢重编程，促进化疗耐药性产生。
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如需具体文献，建议通过PubMed或Google Scholar检索关键词 **"TLX3 recombinant protein"** 或 **"TLX3 structure/function"**，并筛选近5-10年发表的高被引论文。
TLX3 (T-cell leukemia homeobox 3) is a member of the homeobox transcription factor family, characterized by a conserved DNA-binding homeodomain that regulates gene expression during embryonic development. It plays critical roles in neuronal differentiation, dorsal spinal cord patterning, and hematopoietic lineage specification. In normal physiology, TLX3 is transiently expressed in restricted tissues, notably the developing nervous system and immature hematopoietic cells. However, its dysregulation is strongly linked to T-cell acute lymphoblastic leukemia (T-ALL), where chromosomal rearrangements (e.g., t(5;14)(q35;q32)) position TLX3 under the control of potent enhancers, causing aberrant overexpression. This ectopic expression blocks T-cell maturation, promotes leukemogenesis by sustaining progenitor-like proliferation, and is considered an oncogenic driver in 5-10% of pediatric T-ALL cases.
Recombinant human TLX3 protein, typically produced in Escherichia coli or mammalian expression systems, retains the conserved homeodomain structure and DNA-binding capacity. It serves as a vital tool for studying TLX3’s molecular interactions, transcriptional targets (e.g., *PTGFRN*, *ROR1*), and chromatin remodeling effects. Researchers utilize purified TLX3 protein in electrophoretic mobility shift assays, structural studies (e.g., X-ray crystallography), and functional analyses to explore its role in both developmental biology and malignancy. Its application extends to drug screening platforms aiming to inhibit TLX3-driven transcriptional programs in leukemia therapeutics.
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