纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | SH3BP5 |
Uniprot No | O60239 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-455 aa |
活性数据 | MDAALKRSRS EEPAEILPPA RDEEEEEEEG MEQGLEEEEE VDPRIQGELE KLNQSTDDIN RRETELEDAR QKFRSVLVEA TVKLDELVKK IGKAVEDSKP YWEARRVARQ AQLEAQKATQ DFQRATEVLR AAKETISLAE QRLLEDDKRQ FDSAWQEMLN HATQRVMEAE QTKTRSELVH KETAARYNAA MGRMRQLEKK LKRAINKSKP YFELKAKYYV QLEQLKKTVD DLQAKLTLAK GEYKMALKNL EMISDEIHER RRSSAMGPRG CGVGAEGSST SVEDLPGSKP EPDAISVASE AFEDDSCSNF VSEDDSETQS VSSFSSGPTS PSEMPDQFPA VVRPGSLDLP SPVSLSEFGM MFPVLGPRSE CSGASSPECE VERGDRAEGA ENKTSDKANN NRGLSSSSGS GGSSKSQSST SPEGQALENR MKQLSLQCSK GRDGIIADIK MVQIG |
分子量 | 50.4 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. |
以下是关于重组人SH3BP5蛋白的3篇参考文献示例(内容为虚构,仅用于格式展示):
1. **文献名称**: *SH3BP5 regulates mitochondrial apoptosis through JNK signaling*
**作者**: Zhang L, et al.
**摘要**: 研究揭示SH3BP5(SAB)作为线粒体膜蛋白,通过结合JNK激酶调控细胞凋亡,并证实其在氧化应激下激活c-Jun通路的作用机制。
2. **文献名称**: *Structural insights into SH3BP5-mediated stress response*
**作者**: Tanaka K, et al.
**摘要**: 通过晶体学解析SH3BP5的SH3结构域,提出其与Bcl-2家族蛋白互作的新模型,为靶向线粒体凋亡的癌症治疗提供理论基础。
3. **文献名称**: *SH3BP5 deficiency promotes liver cancer progression*
**作者**: Wang Y, et al.
**摘要**: 临床数据表明SH3BP5在肝癌组织中表达下调,实验证明其缺失通过增强线粒体膜通透性导致细胞凋亡抵抗,促进肿瘤发展。
(注:以上文献为示例,实际引用需查阅真实数据库如PubMed。)
SH3BP5. also known as SAB (SH3 domain-binding protein 5), is a mitochondrial outer membrane protein that plays a critical role in regulating cellular apoptosis and mitochondrial dynamics. Initially identified through its interaction with SH3 domain-containing proteins, SH3BP5 serves as a scaffold protein that modulates stress-activated signaling pathways. It is ubiquitously expressed across tissues, with higher levels observed in the liver, heart, and brain. Structurally, SH3BP5 contains conserved SH3-binding motifs and a mitochondrial targeting sequence, enabling its localization to mitochondria.
Functionally, SH3BP5 interacts with kinases such as JNK (c-Jun N-terminal kinase) and Akt/PKB, influencing mitochondrial-dependent apoptosis. It promotes the activation of JNK under stress conditions, leading to cytochrome c release and caspase activation. Conversely, its interaction with Akt can suppress pro-apoptotic signals, highlighting its dual regulatory role. SH3BP5 also participates in maintaining mitochondrial morphology by affecting fission/fusion processes through association with dynamin-related proteins like Drp1.
Recombinant human SH3BP5 protein is widely used to study its biochemical interactions, post-translational modifications, and functional mechanisms in vitro. Dysregulation of SH3BP5 has been linked to diseases such as cancer, neurodegenerative disorders, and metabolic syndromes. In hepatocellular carcinoma, SH3BP5 downregulation correlates with tumor progression, while its overexpression sensitizes cells to apoptosis-inducing therapies. Its emerging role in mitochondrial quality control and stress response pathways positions SH3BP5 as a potential therapeutic target for diseases involving mitochondrial dysfunction.
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