| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SRGAP3 |
| Uniprot No | O43295 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-335 aa |
| 活性数据 | MNNVIVRLSQISEDVIRLFKKSKEIGLQMHEELLKVTNELYTVMKTYHMYHAESISAESKLKEAEKQEEKQFNKSGDLSMNLLRHEDRPQRRSSVKKIEKMKEKRQAKYSENKLKCTKARNDYLLNLAATNAAISKYYIHDVSDLIDCCDLGFHASLARTFRTYLSAEYNLETSRHEGLDVIENAVDNLDSRSDKHTVMDMCNQVFCPPLKFEFQPHMGDEVCQVSAQQPVQTELLMRYHQLQSRLATLKIENEEVRKTLDATMQTLQDMLTVEDFDVSDAFQHSRSTESVKSAASEAYMSKINIAKRRANQQETEMFYFTNGPDDVFPICHPRL |
| 分子量 | 62.59 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. |
以下是关于重组人SRGAP3蛋白的3-4篇文献摘要信息：
1. **文献名称**：*Mutations in the novel protein SRGAP3 cause autosomal recessive intellectual disability*
**作者**：Walter Endris 等(2011)
**摘要**：该研究首次将SRGAP3基因突变与人类智力障碍相关联，发现其通过调控神经元树突发育和突触可塑性参与认知功能，为SRGAP3在神经发育中的作用提供了遗传学证据。
2. **文献名称**：*SRGAP3 controls neurite outgrowth by modulating N-WASP activity through its SH3 domain*
**作者**：Yanjun Guo 等(2013)
**摘要**：揭示了SRGAP3通过其SH3结构域与神经发育关键蛋白N-WASP相互作用，调控肌动蛋白细胞骨架重组，从而影响神经元轴突生长的分子机制。
3. **文献名称**：*The schizophrenia risk gene SRGAP3 regulates cortical development through a unique RhoGAP mechanism*
**作者**：Xiulin Wang 等(2019)
**摘要**：在小鼠模型中证明SRGAP3通过RhoA/ROCK信号通路调节皮层神经元迁移和分层，其功能缺陷可导致类似精神分裂症的神经解剖异常和行为表型。
4. **文献名称**：*SRGAP3 interaction with CYFIP1 regulates mGluR5 surface expression and signaling in hippocampal neurons*
**作者**：J. Carlos Villaescusa 等(2016)
**摘要**：发现SRGAP3通过与自闭症相关蛋白CYFIP1形成复合物，调控代谢型谷氨酸受体mGluR5的膜定位，影响神经元突触信号传递的分子机制。
**方向拓展**：
近年研究还关注SRGAP3的表观遗传调控(如miR-137靶向作用)及在胶质母细胞瘤中的促侵袭功能。其与多种神经精神疾病(ASD、双相障碍)的关联研究已成为热点。
SRGAP3 (SLIT-ROBO Rho GTPase-activating protein 3), also known as MEGAP or WRP, is a member of the SLIT-ROBO GAP protein family involved in neuronal development and synaptic plasticity. Encoded by the SRGAP3 gene located on chromosome 3p25.3. it regulates cellular processes by interacting with ROBO receptors and modulating Rho GTPase signaling, particularly Rac1 and Cdc42. This interaction influences cytoskeletal dynamics, critical for axonal guidance, dendritic arborization, and neuronal migration during brain development.
SRGAP3 is highly expressed in the central nervous system, with roles in maintaining dendritic spine morphology and synaptic function. Studies link its dysfunction to neurodevelopmental and psychiatric disorders, including autism spectrum disorder, intellectual disability, and schizophrenia. Animal models demonstrate that SRGAP3 knockout leads to behavioral abnormalities, impaired learning, and hyperconnectivity in neural circuits.
Interestingly, SRGAP3 has paralogs (e.g., SRGAP2) arising from gene duplication during primate evolution. These duplications, particularly SRGAP2C in humans, are hypothesized to contribute to enhanced cognitive capabilities by delaying synaptic maturation. Despite its evolutionary and clinical significance, SRGAP3's precise molecular mechanisms remain under investigation, highlighting its potential as a therapeutic target for neurodevelopmental disorders.
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