| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SF3B1 |
| Uniprot No | O75533 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 326-571aa |
| 氨基酸序列 | TPTPGASKRKSRWDETPASQMGGSTPVLTPGKTPIGTPAMNMATPTPGHIMSMTPEQLQAWRWEREIDERNRPLSDEELDAMFPEGYKVLPPPAGYVPIRTPARKLTATPTPLGGMTGFHMQTEDRTMKSVNDQPSGNLPFLKPDDIQYFDKLLVDVDESTLFPEEQKERKIMKLLLKIKNGTPPMRKAALRQITDKAREFGAGPLFNQILPLLMSPTLEDQERHLLVKVIDRILYKLDDLVRPYV |
| 预测分子量 | 33.8 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SF3B1重组蛋白的3篇参考文献，按文献名称、作者和摘要内容概括列出：
1. **"Frequent pathway mutations of splicing machinery in myelodysplasia"**
*作者*：Yoshida K, et al. (2011)
*摘要*：该研究首次发现SF3B1基因在骨髓增生异常综合征(MDS)中的高频突变，揭示了SF3B1突变导致RNA剪接异常，影响造血干细胞的正常功能，并与疾病预后相关。
2. **"Cancer-Associated SF3B1 Mutations Alter RNA Splicing by Enhancing Branch Site Recognition"**
*作者*：Darman RB, et al. (2015)
*摘要*：本文阐明了SF3B1突变通过异常识别mRNA前体的分支位点(branchpoint)，导致错误剪接事件的累积，促进癌症发生发展的分子机制。
3. **"SF3B1 mutations are associated with specific alternative splicing patterns in myelodysplastic syndromes"**
*作者*：Visconte V, et al. (2012)
*摘要*：研究分析了MDS患者中SF3B1突变的剪接异常特征，发现突变导致3'剪接位点(3' splice site)选择偏移，生成异常转录本，可能与铁代谢相关基因异常有关。
4. **"Mutant SF3B1 promotes malignancy in chronic lymphocytic leukemia via altered pre-mRNA splicing"**
*作者*：Seiler M, et al. (2018)
*摘要*：该研究揭示了慢性淋巴细胞白血病(CLL)中SF3B1突变通过改变剪接体功能，影响DNA损伤修复通路(如BRCA1/2相关基因)，进而促进肿瘤进展，并提出靶向剪接体抑制剂(如E7107)的治疗潜力。
---
以上文献均聚焦于SF3B1突变在RNA剪接中的分子机制及其在血液系统恶性肿瘤中的病理作用。
SF3B1 is a critical component of the spliceosome, a dynamic molecular machinery responsible for removing introns from precursor messenger RNA (pre-mRNA) during eukaryotic gene expression. As part of the U2 small nuclear ribonucleoprotein (snRNP) complex, SF3B1 plays a key role in recognizing branch site sequences and ensuring accurate splice site selection. Recombinant SF3B1 protein, produced through genetic engineering techniques in systems like bacteria, yeast, or mammalian cells, enables detailed biochemical and structural studies of its function in RNA splicing.
Mutations in SF3B1 are frequently observed in cancers (e.g., myelodysplastic syndromes, chronic lymphocytic leukemia) and are linked to aberrant mRNA splicing, which promotes tumorigenesis by generating oncogenic isoforms. Recombinant SF3B1 proteins, often tagged with fluorescent or affinity markers, facilitate investigations into these pathogenic mechanisms. Researchers use them to analyze interactions with splicing factors, study the effects of cancer-associated mutations, and screen for small-molecule inhibitors targeting spliceosome activity.
Notably, SF3B1 has emerged as a therapeutic target, with compounds like pladienolide derivatives (e.g., E7107) and H3B-8800 designed to modulate its function. Structural studies using recombinant SF3B1. combined with cryo-EM, have revealed binding sites for these inhibitors, advancing drug development. Additionally, recombinant proteins aid in deciphering SF3B1's role in maintaining genomic stability and cellular stress responses. Its study provides insights into both fundamental splicing mechanisms and therapeutic strategies for splicing factor-related diseases.
×
