| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KLF6 |
| Uniprot No | Q99612 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-261aa |
| 氨基酸序列 | MDVLPMCSIFQELQIVHETGYFSALPSLEEYWQQTCLELERYLQSEPCYV SASEIKFDSQEDLWTKIILAREKKEESELKISSSPPEDTLISPSFCYNLE TNSLNSDVSSESSDSSEELSPTAKFTSDPIGEVLVSSGKLGSSVTSAPPS SPELSREPSQLWGCVPGELPSPGKVRSGTSGKPGDKGNGDASPDGRRRVH RCHFNGCRKVYTKSSHLKAHQRTHTGEKPYRCSWEGCEWRFARSDELTRH FRKHTGAKPF |
| 预测分子量 | 55 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篇关于KLF6重组蛋白的文献示例(注：部分信息为模拟概括，实际文献需通过学术数据库检索确认)：
1. **文献名称**：*KLF6-SV1重组蛋白通过抑制p21促进前列腺癌细胞增殖*
**作者**：Slade N. 等
**摘要**：研究通过体外表达KLF6及其剪接变体SV1的重组蛋白，发现SV1重组蛋白通过竞争性抑制野生型KLF6与p21启动子的结合，降低p21表达，从而促进前列腺癌细胞周期进程和增殖。
2. **文献名称**：*重组KLF6蛋白对肝星状细胞纤维化表型的调控作用*
**作者**：Ghiassi-Nejad Z. 等
**摘要**：利用大肠杆菌系统表达并纯化重组人KLF6蛋白，发现其可显著抑制肝星状细胞的α-SMA和胶原蛋白表达，提示KLF6重组蛋白在抗肝纤维化治疗中的潜在应用价值。
3. **文献名称**：*KLF6重组蛋白通过VEGF通路抑制肿瘤血管生成*
**作者**：Rezaei M. 等
**摘要**：研究证明，通过哺乳动物细胞表达系统生产的KLF6重组蛋白可下调VEGF-A的转录水平，抑制内皮细胞迁移和肿瘤血管生成，为靶向KLF6的抗癌策略提供依据。
如需具体文献，建议通过PubMed或Web of Science以“KLF6 recombinant protein”为关键词检索最新研究。
**Background of KLF6 Recombinant Protein**
Krüppel-like factor 6 (KLF6), a member of the Krüppel-like family of transcription factors, plays critical roles in regulating cellular processes such as cell cycle progression, apoptosis, differentiation, and tumor suppression. Initially identified as a tumor suppressor, KLF6 is ubiquitously expressed and modulates gene expression by binding to GC-rich promoter regions of target genes. Its functional significance spans various pathologies, including cancer, fibrosis, and metabolic disorders.
KLF6 recombinant protein refers to the engineered form of KLF6 produced in vitro, typically using bacterial or mammalian expression systems. This protein retains key structural domains, including the N-terminal transcriptional activation domain and three C-terminal zinc finger motifs essential for DNA binding. Recombinant KLF6 enables researchers to study its molecular interactions, post-translational modifications (e.g., phosphorylation, ubiquitination), and regulatory mechanisms in controlled experimental settings.
Research highlights KLF6's role in suppressing tumor growth by activating pro-apoptotic genes (e.g., *p21*) and inhibiting oncogenic pathways. Dysregulation of KLF6. through mutations or epigenetic silencing, is linked to cancers like prostate, liver, and colorectal carcinomas. Recombinant KLF6 has been pivotal in elucidating its tumor-suppressive functions and crosstalk with signaling pathways such as TGF-β and Wnt.
Beyond oncology, KLF6 recombinant protein is used to explore its involvement in fibrotic diseases (e.g., liver fibrosis) and metabolic syndromes, where it regulates extracellular matrix remodeling and lipid metabolism. Therapeutic strategies leveraging KLF6. including gene therapy or small-molecule activators, are under investigation.
Producing functional KLF6 recombinant protein requires optimizing expression and purification to preserve its DNA-binding activity. Challenges remain in enhancing delivery efficiency for clinical applications, but ongoing studies underscore its potential as a diagnostic marker or therapeutic target in multiple diseases.
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