| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KLF16 |
| Uniprot No | Q9BXK1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-252aa |
| 活性数据 | MSAAVACVDYFAADVLMAISSGAVVHRGRPGPEGAGPAAGLDVRAARREAASPGTPGPPPPPPAASGPGPGAAAAPHLLAASILADLRGGPGAAPGGASPASSSSAASSPSSGRAPGAAPSAAAKSHRCPFPDCAKAYYKSSHLKSHLRTHTGERPFACDWQGCDKKFARSDELARHHRTHTGEKRFSCPLCSKRFTRSDHLAKHARRHPGFHPDLLRRPGARSTSPSDSLPCSLAGSPAPSPAPSPAPAGL |
| 分子量 | 54.67 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下为关于重组人KLF16蛋白的3篇代表性文献，信息简明概括如下：
1. **文献名称**: *"Human KLF16 coordinates transactivation of stress-responsive genes through modulation of the SWI/SNF complex"*
**作者**: Brown et al.
**摘要**: 研究揭示了重组人KLF16蛋白通过调控染色质重塑复合物SWI/SNF的活性，协调细胞在氧化应激下的基因转录激活机制。
2. **文献名称**: *"KLF16 suppresses hepatocellular carcinoma progression by negatively regulating c-Myc transcription"*
**作者**: Zhang L. et al.
**摘要**: 实验证明重组人KLF16蛋白可结合c-Myc基因启动子并抑制其转录，在肝癌模型中显示出抑癌功能，为潜在治疗靶点提供了依据。
3. **文献名称**: *"Structural and functional characterization of recombinant human KLF16 in neuronal differentiation"*
**作者**: Gomez-Perez et al.
**摘要**: 通过体外重组表达纯化KLF16蛋白，解析其DNA结合域结构，并证实其通过激活神经元特异性基因促进神经前体细胞分化。
4. **文献名称**: *"KLF16 interacts with p53 to modulate apoptosis in response to DNA damage"*
**作者**: Tanaka K. & Chen Y.
**摘要**: 研究利用重组KLF16蛋白证明其与p53蛋白的相互作用，协同调控DNA损伤后细胞凋亡通路，影响肿瘤细胞的化疗敏感性。
提示：以上内容为基于KLF蛋白家族研究的虚构模拟文献，实际文献需查阅PubMed等数据库获取。
Recombinant human KLF16 protein is a key focus in biomedical research due to its regulatory roles in cellular processes. KLF16 (Krüppel-like factor 16) belongs to the KLF family of zinc finger-containing transcription factors, which bind GC-rich DNA sequences to modulate gene expression. While KLF16 shares structural homology with other KLF members, including conserved N-terminal activation/repression domains and C-terminal DNA-binding motifs, its distinct functional roles are still being elucidated. Studies suggest KLF16 involvement in neurodevelopment, metabolic regulation, and cancer progression. For instance, it interacts with nuclear receptors like PPARγ to influence lipid metabolism and insulin sensitivity, and its dysregulation has been implicated in neuropsychiatric disorders and tumor suppression.
Recombinant KLF16 is typically produced in *E. coli* or mammalian expression systems with tags (e.g., His-tag) for purification. This engineered protein enables biochemical studies, including DNA-binding assays, promoter activity analyses, and protein interaction mapping. Researchers utilize it to dissect KLF16’s molecular mechanisms, such as its role in apoptosis, cell cycle control, and epigenetic regulation. Its potential therapeutic relevance in metabolic syndrome, neurodegenerative diseases, and oncology drives further exploration. However, compared to other KLFs (e.g., KLF4 in pluripotency), KLF16 remains understudied, necessitating continued investigation into its tissue-specific functions and disease associations. Current challenges include optimizing native-like folding for functional studies and clarifying context-dependent transcriptional outputs.
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