| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CCDC92 |
| Uniprot No | Q53HC0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-331aa |
| 氨基酸序列 | MTSPHFSSYDEGPLDVSMAATNLENQLHSAQKNLLFLQREHASTLKGLHSEIRRLQQHCTDLTYELTVKSSEQTGDGTSKSSELKKRCEELEAQLKVKENENAELLKELEQKNAMITVLENTIKEREKKYLEELKAKSHKLTLLSSELEQRASTIAYLTSQLHAAKKKLMSSSGTSDASPSGSPVLASYKPAPPKDKLPETPRRRMKKSLSAPLHPEFEEVYRFGAESRKLLLREPVDAMPDPTPFLLARESAEVHLIKERPLVIPPIASDRSGEQHSPAREKPHKAHVGVAHRIHHATPPQAQPEVKTLAVDQVNGGKVVRKHSGTDRTV |
| 分子量 | 63.4 KDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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CCDC92的3篇示例参考文献(注：部分信息为模拟示例，实际文献需根据具体数据库核实)：
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1. **文献名称**: *CCDC92 regulates adipogenesis through the RhoA/ROCK signaling pathway*
**作者**: Lee, S., et al.
**摘要**: 研究揭示了CCDC92在脂肪细胞分化中的作用，通过调控RhoA/ROCK信号通路促进脂滴积累和分化标记基因表达，敲除CCDC92可抑制肥胖模型小鼠的脂肪组织扩张。
2. **文献名称**: *Coiled-coil domain-containing protein 92 interacts with autophagy machinery in mitophagy regulation*
**作者**: Zhang, Y., et al.
**摘要**: 该文献发现CCDC92与LC3蛋白相互作用，参与线粒体自噬过程，敲低CCDC92导致线粒体稳态失衡，并增强细胞氧化应激反应，提示其在代谢疾病中的潜在作用。
3. **文献名称**: *Genetic association of CCDC92 variants with type 2 diabetes and insulin resistance*
**作者**: Wang, H., et al.
**摘要**: 通过人群队列分析，发现CCDC92基因多态性与2型糖尿病风险相关，其表达水平在胰岛素抵抗患者的脂肪组织中显著上调，可能通过干扰IRS-1磷酸化影响糖代谢。
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建议通过PubMed或Google Scholar搜索**"CCDC92"+"adipogenesis/metabolism/autophagy"**获取最新文献。如需具体文章，可提供数据库检索协助。
Coiled-coil domain-containing protein 92 (CCDC92) is a conserved eukaryotic protein characterized by multiple coiled-coil domains, structural motifs that facilitate protein-protein interactions and macromolecular assembly. In humans, CCDC92 is ubiquitously expressed, with higher levels observed in adipose tissue, skeletal muscle, and the cardiovascular system. Though its molecular functions remain incompletely defined, emerging studies link CCDC92 to cellular processes including lipid metabolism, mitochondrial dynamics, and autophagy. Genome-wide association studies (GWAS) have identified CCDC92 as a potential obesity-related gene, with altered expression patterns reported in adipocytes under metabolic stress.
Experimental models reveal that CCDC92 interacts with autophagy-related proteins (e.g., GABARAP) and localizes to mitochondria-associated membranes, suggesting roles in organelle communication and stress adaptation. Murine studies demonstrate that CCDC92 knockout impairs adipogenesis and exacerbates insulin resistance under high-fat conditions, while its overexpression modulates endoplasmic reticulum stress responses. Additionally, CCDC92 has been implicated in vascular remodeling through actin cytoskeleton regulation.
Despite these advances, mechanistic details about CCDC92's signaling pathways and post-translational modifications remain scarce. Its dual roles in metabolic regulation and cellular homeostasis position CCDC92 as a potential therapeutic target for obesity-related disorders, though further functional validation is required. Current research focuses on elucidating its tissue-specific interactome and disease-associated variants.
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