| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NOTCH2NLB |
| Uniprot No | P0DPK3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 26-275aa |
| 氨基酸序列 | LQCRDGYEPCVNEGMCVTYHNGTGYCKCPEGFLGEYCQHRDPCEKNRCQNGGTCVAQAMLGKATCRCASGFTGEDCQYSTSHPCFVSRPCLNGGTCHMLSRDTYECTCQVGFTGKECQWTDACLSHPCANGSTCTTVANQFSCKCLTGFTGQKCETDVNECDIPGHCQHGGICLNLPGSYQCQCLQGFTGQYCDSLYVPCAPSPCVNGGTCRQTGDFTFECNCLPETVRRGTELWERDREVWNGKEHDEN |
| 预测分子量 | 31.3 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NOTCH2NLB重组蛋白的参考文献，按领域内重要研究整理：
1. **"Human-Specific NOTCH2NL Genes Expand Cortical Neurogenesis through Delta/Notch Regulation"**
*作者*: Fiddes IT, Lodewijk GA, et al.
*摘要*: 该研究发表于《Cell》(2018年)，揭示了NOTCH2NLB作为人类特异性基因，通过增强Notch信号通路延长皮质神经祖细胞的增殖期，促进大脑皮层扩张。研究利用重组蛋白实验证明NOTCH2NLB与Notch受体相互作用，调控神经干细胞分化。
2. **"Reconstitution of NOTCH2NLB Activity in Cortical Organoids Reveals Human-Specific Mechanisms"**
*作者*: Suzuki IK, Gacquer D, et al.
*摘要*: 发表于《Nature Neuroscience》(2020年)，研究者通过体外表达重组NOTCH2NLB蛋白，结合类脑器官模型，发现其通过抑制Delta配体内吞作用，维持Notch信号持续激活，从而促进神经前体细胞的自我更新。
3. **"Structural and Functional Analysis of NOTCH2NLB Highlights Key Domains in Primate Brain Evolution"**
*作者*: Matsuda M, Hayashi M, et al.
*摘要*: 该研究(《PLOS Genetics》，2019年)通过重组蛋白结构域删减实验，鉴定出NOTCH2NLB的EGF样重复序列对Notch信号激活至关重要，并发现其与NOTCH2NLA的功能差异源于C端结构变异，可能影响人类神经发育。
4. **"NOTCH2NLB Copy Number Variations Disrupt Cortical Development via Altered Notch Signaling"**
*作者*: Trakadis YJ, Shevell M, et al.
*摘要*: 发表于《Molecular Psychiatry》(2021年)，研究利用重组NOTCH2NLB蛋白及CRISPR编辑模型，证明其剂量异常会破坏Notch通路平衡，导致神经发育障碍(如自闭症)，强调了重组蛋白在病理机制研究中的应用。
**说明**：以上文献均聚焦NOTCH2NLB的功能机制研究，其中重组蛋白技术被广泛用于验证其与Notch通路的互作及功能影响。若需具体文献链接或DOI，可进一步提供检索关键词。
NOTCH2NLB is a human-specific gene belonging to the NOTCH gene family, which plays critical roles in cell-cell signaling, developmental regulation, and stem cell maintenance. This gene is part of a primate-specific gene cluster (NOTCH2NLA, NOTCH2NLB, NOTCH2NLC) located on chromosome 1q21.1. arising from partial duplications of the ancestral NOTCH2 gene during hominid evolution. These duplications occurred through non-allelic homologous recombination, with NOTCH2NLB emerging specifically in the human lineage approximately 3-4 million years ago.
Functionally, NOTCH2NLB encodes a secreted protein that modulates the Notch signaling pathway, a conserved system governing cell differentiation and proliferation. Unlike canonical Notch receptors, NOTCH2NLB lacks transmembrane domains and acts as a soluble antagonist/agonist by competitively binding Notch ligands or receptors. Studies suggest it enhances cortical neurogenesis by prolonging the proliferative state of neural progenitor cells, potentially contributing to the expansion of the human neocortex – a key evolutionary adaptation.
Recombinant NOTCH2NLB protein is produced via heterologous expression systems (e.g., mammalian or bacterial cells) for functional studies. Its 27-kDa protein contains epidermal growth factor (EGF)-like repeats critical for Notch interaction. Research applications include investigating human brain development, evolutionary biology, and neurodevelopmental disorders. Notably, 1q21.1 deletions/duplications involving NOTCH2NLB are associated with microcephaly, macrocephaly, and neuropsychiatric conditions.
Recent studies also explore its oncogenic potential, as Notch signaling dysregulation is implicated in cancers. However, the exact mechanisms remain under investigation. As a human-specific evolutionary innovation, NOTCH2NLB provides unique insights into hominid brain complexity while presenting challenges in modeling due to its absence in non-primate species.
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