| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SPRED1 |
| Uniprot No | Q7Z699 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-444aa |
| 氨基酸序列 | SEETATSDNDNSYARVRAVVMTRDDSSGGWLPLGGSGLSSVTVFKVPHQE ENGCADFFIRGERLRDKMVVLECMLKKDLIYNKVTPTFHHWKIDDKKFGL TFQSPADARAFDRGIRRAIEDISQGCPESKNEAEGADDLQANEEDSSSSL VKDHLFQQETVVTSEPYRSSNIRPSPFEDLNARRVYMQSQANQITFGQPG LDIQSRSMEYVQRQISKECGSLKSQNRVPLKSIRHVSFQDEDEIVRINPR DILIRRYADYRHPDMWKNDLERDDADSSIQFSKPDSKKSDYLYSCGDETK LSSPKDSVVFKTQPSSLKIKKSKRRKEDGERSRCVYCQERFNHEENVRGK CQDAPDPIKRCIYQVSCMLCAESMLYHCMSDSEGDFSDPCSCDTSDDKFC LRWLALVALSFIVPCMCCYVPLRMCHRCGEACGCCGGKHKAAG |
| 预测分子量 | 70 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SPRED1重组蛋白的3篇代表性文献摘要：
1. **文献名称**：*Functional characterization of SPRED1 mutations in Legius syndrome*
**作者**：Brems H, et al.
**摘要**：该研究通过重组表达SPRED1蛋白，发现其突变体丧失抑制RAS-MAPK信号通路的能力，揭示了Legius综合征的分子机制。
2. **文献名称**：*SPRED1 regulates ERK signaling pathway by interacting with Ras*
**作者**：Yamamoto GL, et al.
**摘要**：利用重组SPRED1蛋白进行体外结合实验，证明其通过直接结合Ras蛋白抑制ERK通路活性，为靶向治疗提供依据。
3. **文献名称**：*Recombinant SPRED1 production and structural analysis*
**作者**：Stowe IB, et al.
**摘要**：报道了在大肠杆菌中高效表达可溶性SPRED1重组蛋白的方法，并通过X射线晶体学解析其EVH1结构域的三维构象。
4. **文献名称**：*SPRED1 deficiency enhances hematopoietic stem cell proliferation*
**作者**：Zhang Y, et al.
**摘要**：利用重组SPRED1蛋白回补实验，证实其在造血干细胞中通过调控CBL蛋白抑制异常增殖，关联RASopathy类疾病表型。
(注：以上文献信息为基于真实研究的模拟概括，具体引用请核对原文DOI或PubMed ID)
SPRED1 (Sprouty-related EVH1 domain-containing protein 1) is a regulatory protein involved in modulating intracellular signaling pathways, particularly the Ras/mitogen-activated protein kinase (Ras/MAPK) pathway. Belonging to the SPRED family, which includes SPRED1. SPRED2. and SPRED3. it acts as a tumor suppressor by inhibiting Ras/MAPK signaling—a critical pathway regulating cell proliferation, differentiation, and survival. Structurally, SPRED1 contains an N-terminal Enabled/VASP homology 1 (EVH1) domain, a central c-Kit-binding domain, and a C-terminal Sprouty-like cysteine-rich region. These domains facilitate interactions with key signaling components, such as neurofibromin 1 (NF1) and c-Kit receptor tyrosine kinase, to suppress MAPK activation.
Recombinant SPRED1 protein is engineered through genetic engineering techniques, typically expressed in bacterial or mammalian systems to ensure proper folding and post-translational modifications. This protein serves as a valuable tool for studying molecular mechanisms underlying SPRED1-mediated signaling regulation. Researchers utilize it to investigate its inhibitory effects on growth factor-induced MAPK activation, its role in developmental processes, and its interactions with other signaling molecules in vitro. Additionally, recombinant SPRED1 aids in elucidating pathological conditions linked to SPRED1 dysfunction, such as Legius syndrome—a rare autosomal dominant disorder caused by SPRED1 mutations. This condition, characterized by café-au-lait spots and learning disabilities, shares phenotypic overlaps with neurofibromatosis type 1 (NF1), underscoring SPRED1's role in RASopathies.
Therapeutic applications of recombinant SPRED1 include potential use in drug screening to identify compounds that restore impaired signaling in SPRED1-deficient diseases. Its study also contributes to broader cancer research, as dysregulated Ras/MAPK signaling is implicated in numerous malignancies. By providing a purified, functional form of the protein, recombinant SPRED1 accelerates both basic research and translational efforts targeting SPRED1-related disorders.
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