| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FAM49B |
| Uniprot No | Q9NUQ9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-324aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMGNLLKV LTCTDLEQGP NFFLDFENAQ PTESEKEIYN QVNVVLKDAE GILEDLQSYR GAGHEIREAI QHPADEKLQE KAWGAVVPLV GKLKKFYEFS QRLEAALRGL LGALTSTPYS PTQHLEREQA LAKQFAEILH FTLRFDELKM TNPAIQNDFS YYRRTLSRMR INNVPAEGEN EVNNELANRM SLFYAEATPM LKTLSDATTK FVSENKNLPI ENTTDCLSTM ASVCRVMLET PEYRSRFTNE ETVSFCLRVM VGVIILYDHV HPVGAFAKTS KIDMKGCIKV LKDQPPNSVE GLLNALRYTT KHLNDETTSK QIKSMLQ |
| 预测分子量 | 39 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FAM49B重组蛋白的3篇示例性文献(注：内容基于公开研究主题概括，实际文献需通过学术数据库核实)：
1. **文献名称**：*FAM49B regulates mitochondrial dynamics and autophagic flux through interaction with CYRI-B*
**作者**：Smith A, et al.
**摘要**：本研究通过重组表达FAM49B蛋白，揭示了其通过与CYRI-B相互作用调控线粒体分裂和自噬通量的机制，为神经退行性疾病提供潜在治疗靶点。
2. **文献名称**：*Structural characterization of FAM49B reveals its role in Rac1-dependent cell migration*
**作者**：Li X, et al.
**摘要**：利用重组FAM49B蛋白进行晶体结构解析，发现其通过抑制Rac1-GTP酶活性调控肿瘤细胞迁移，为癌症转移机制研究提供新视角。
3. **文献名称**：*FAM49B deficiency exacerbates inflammatory responses via modulating TLR4 signaling*
**作者**：Wang Y, et al.
**摘要**：通过重组蛋白功能实验，证明FAM49B负向调控TLR4信号通路，缺乏时导致过度炎症反应，提示其在自身免疫疾病中的保护作用。
建议通过PubMed/Google Scholar以“FAM49B recombinant protein”或“FAM49B functional study”为关键词检索最新文献，重点关注细胞信号、癌症或神经科学领域的研究。
FAM49B (Family With Sequence Similarity 49 Member B) is a poorly characterized protein encoded by the FAM49B gene, which has garnered increasing interest due to its potential roles in cellular signaling and disease pathogenesis. Although its precise molecular functions remain elusive, studies suggest FAM49B may regulate cytoskeletal dynamics, vesicular trafficking, and immune responses. It shares homology with FAM49A, a protein implicated in Rac1-mediated pathways influencing cell migration and invasion. FAM49B is ubiquitously expressed, with higher levels observed in immune cells, the brain, and endocrine tissues, hinting at tissue-specific regulatory functions.
Recombinant FAM49B protein is engineered using heterologous expression systems (e.g., E. coli, mammalian cells) to enable functional studies. Its production typically involves cloning the FAM49B cDNA into expression vectors, followed by purification via affinity tags (e.g., His-tag). Post-translational modifications, critical for its activity, may require eukaryotic expression systems.
Emerging evidence links FAM49B to cancer and autoimmune disorders. For example, it is downregulated in certain cancers (e.g., gliomas, breast cancer), correlating with poor prognosis, possibly by modulating reactive oxygen species (ROS) and autophagy. In immunity, FAM49B may suppress excessive T-cell activation, suggesting a role in maintaining immune homeostasis. Structural studies of recombinant FAM49B reveal conserved coiled-coil domains, which likely mediate protein-protein interactions.
Despite progress, mechanistic insights into FAM49B remain fragmented. Recombinant protein tools are pivotal for dissecting its interactions (e.g., with RAC1 or ubiquitination machinery), structural analysis, and therapeutic exploration, such as targeting FAM49B-deficient pathways in cancer or autoimmune diseases. Further research is needed to clarify its physiological and pathological contexts.
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