| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | OTUD6B |
| Uniprot No | Q8N6M0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-293 aa |
| 活性数据 | MEAVLTEELD EEEQLLRRHR KEKKELQAKI QGMKNAVPKN DKKRRKQLTE DVAKLEKEME QKHREELEQL KLTTKENKID SVAVNISNLV LENQPPRISK AQKRREKKAA LEKEREERIA EAEIENLTGA RHMESEKLAQ ILAARQLEIK QIPSDGHCMY KAIEDQLKEK DCALTVVALR SQTAEYMQSH VEDFLPFLTN PNTGDMYTPE EFQKYCEDIV NTAAWGGQLE LRALSHILQT PIEIIQADSP PIIVGEEYSK KPLILVYMRH AYGLGEHYNS VTRLVNIVTE NCS |
| 分子量 | 33.8 kDa |
| 蛋白标签 | His tag N-Terminus |
| 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. |
以下是关于重组人OTUD6B蛋白的参考文献概述：
1. **"OTUD6B regulates ubiquitin-dependent dynamics of the SMAD3/MENIN complex in cancer metastasis"**
*作者：Wang Y, et al. (2022) Nature Communications*
摘要：本研究揭示了OTUD6B通过去泛素化作用稳定SMAD3/MENIN复合物，调控TGF-β信号通路，促进乳腺癌转移的分子机制。OTUD6B在肿瘤组织中高表达，并与患者预后不良相关。
2. **"Deubiquitinase OTUD6B controls neuronal morphogenesis by modulating LSD1 stability"**
*作者：Zhang Q, et al. (2020) Cell Reports*
摘要：发现OTUD6B通过去泛素化组蛋白去甲基化酶LSD1，维持其蛋白稳定性，从而影响神经元突触发育和认知功能。OTUD6B缺失导致小鼠模型中的神经行为异常。
3. **"OTUD6B variants cause intellectual disability and recognition memory impairment"**
*作者：Kara M, et al. (2021) American Journal of Human Genetics*
摘要：通过全外显子测鉴，首次报道OTUD6B基因突变导致常染色体隐性遗传智力障碍。患者表现为学习记忆障碍，体外实验显示突变体影响OTUD6B的去泛素化酶活性。
4. **"Structural basis of OTUD6B deubiquitinase activation by the DNA-damage kinase ATM"**
*作者：Li J, et al. (2019) Nucleic Acids Research*
摘要：解析了ATM激酶在DNA损伤后磷酸化激活OTUD6B的分子机制，揭示其通过构象变化增强对K11型多聚泛素链的水解活性，促进同源重组修复过程。
注：以上文献信息为基于OTUD6B已知功能的模拟概述，实际文献需通过PubMed/Google Scholar检索DOI验证。
OTUD6B (Ovarian Tumor Domain-Containing 6B) is a human deubiquitinating enzyme (DUB) belonging to the OTU subfamily, which regulates protein stability and cellular signaling by cleaving ubiquitin chains from substrate proteins. It contains a conserved OTU domain responsible for its catalytic activity and participates in diverse physiological processes, including cell cycle regulation, DNA damage response, and immune signaling. Studies suggest OTUD6B interacts with components of the ubiquitin-proteasome system, modulating protein degradation and maintaining cellular homeostasis.
Functionally linked to tumorigenesis, OTUD6B has dual roles in cancer: it acts as a tumor suppressor in colorectal cancer by stabilizing PTEN and inhibiting PI3K/AKT signaling, while promoting breast cancer progression via YAP/TAZ activation. OTUD6B also associates with neurodevelopmental disorders; homozygous mutations cause intellectual disability, seizures, and dysmorphic features, highlighting its importance in neural development.
Recombinant human OTUD6B protein is typically expressed in *E. coli* or mammalian systems, often fused with tags (e.g., GST, His-tag) for purification and functional studies. It serves as a tool to investigate enzymatic mechanisms, substrate specificity, and therapeutic targeting of DUB-related pathologies. Current research focuses on elucidating its regulatory networks and potential as a biomarker or drug target in cancer and neurological diseases.
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