纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | RAD54B |
Uniprot No | Q9Y620 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-158 aa |
活性数据 | MLDHHPVAITVEVKQEEDIKPPPPLVLNSQQSDTLEQREEHELVHVMERSLSPSLSSVDMRMTSSPSSIPRRDDFFRHESGEHFRSLLGYDPQILQMLKEEHQIILENQKNFGLYVQEKRDGLKRRQQLEEELLRAKIEVEKLKAIRLRHDLPEYNSL |
分子量 | 45 kDa |
蛋白标签 | GST-tag at N-terminal |
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. |
1. **"RAD54B promotes repair of Cas9-induced DNA breaks in human cells"**
作者:Bétermier et al.
摘要:该研究探讨RAD54B在CRISPR/Cas9诱导的DNA双链断裂修复中的作用,发现其通过促进同源重组修复路径增强断裂位点的修复效率,同时减少非同源末端连接的比例。
2. **"RAD54B modulates homologous recombination by disrupting RAD51-DNA filaments"**
作者:Mazin et al.
摘要:揭示了RAD54B通过调控RAD51蛋白在DNA损伤位点的组装与解离,优化同源重组修复过程,其解旋酶活性对维持基因组稳定性至关重要。
3. **"RAD54B deficiency predisposes to myelodysplastic syndrome via impaired DNA repair"**
作者:Shah et al.
摘要:通过小鼠模型和患者样本分析,发现RAD54B缺失导致造血干细胞DNA修复缺陷,增加骨髓异常增生综合征(MDS)风险,提示其作为潜在肿瘤抑制因子。
4. **"Structural insights into RAD54B's role in chromatin remodeling during homologous recombination"**
作者:Watanabe & Hashimoto
摘要:结合冷冻电镜技术,解析RAD54B与核小体复合物的结构,阐明其通过重塑染色质结构协助RAD51介导的DNA链侵入与配对机制。
RAD54B is a member of the RAD54 family of DNA helicases, which belong to the Swi2/Snf2 ATPase superfamily. It plays a critical role in homologous recombination repair (HR), a high-fidelity pathway essential for resolving DNA double-strand breaks (DSBs) and maintaining genomic stability. RAD54B functions as an ATP-dependent chromatin remodeler, working cooperatively with RAD51 recombinase to facilitate homology search, strand pairing, and displacement loop (D-loop) formation during HR. Its enzymatic activity enhances RAD51-mediated strand exchange by modulating chromatin structure and stabilizing recombination intermediates.
Mutations or dysregulation of RAD54B are associated with genomic instability, cancer predisposition, and impaired meiosis. Studies link RAD54B deficiency to increased sensitivity to DNA-damaging agents (e.g., ionizing radiation) and synthetic lethality with defects in BRCA1/2 or other HR components, highlighting its therapeutic relevance. In cancer, RAD54B expression patterns may serve as a biomarker for HR proficiency, influencing responses to PARP inhibitors or platinum-based therapies.
Structurally, RAD54B contains conserved helicase domains that bind ATP and translocate along duplex DNA, a feature critical for its role in recombination. Despite functional overlap with its paralog RAD54L, RAD54B exhibits distinct expression profiles and may specialize in repairing specific DNA lesions. Ongoing research explores its interplay with other repair proteins and potential as a target for precision oncology strategies.
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