| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | B4GALT5 |
| Uniprot No | O43286 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-388aa |
| 氨基酸序列 | MRARRGLLRLPRRSLLAALFFFSLSSSLLYFVYVAPGIVNTYLFMMQAQGILIRDNVRTIGAQVYEQVLRSAYAKRNSSVNDSDYPLDLNHSETFLQTTTFLPEDFTYFANHTCPERLPSMKGPIDINMSEIGMDYIHELFSKDPTIKLGGHWKPSDCMPRWKVAILIPFRNRHEHLPVLFRHLLPMLQRQRLQFAFYVVEQVGTQPFNRAMLFNVGFQEAMKDLDWDCLIFHDVDHIPESDRNYYGCGQMPRHFATKLDKYMYLLPYTEFFGGVSGLTVEQFRKINGFPNAFWGWGGEDDDLWNRVQNAGYSVSRPEGDTGKYKSIPHHHRGEVQFLGRYALLRKSKERQGLDGLNNLNYFANITYDALYKNITVNLTPELAQVNEY |
| 分子量 | 45.1 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | 冻干粉 |
| 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. |
以下为3条关于B4GALT5的参考文献信息示例(*注：内容为模拟概括，非真实文献*)
1. **文献名称**：*B4GALT5-mediated glycosylation drives integrin signaling and cancer metastasis*
**作者**：Chen L. et al.
**摘要**：研究发现B4GALT5通过调控β1整合素的半乳糖基化修饰，增强癌细胞与细胞外基质的黏附，激活FAK/Src信号通路，促进肿瘤侵袭和转移。
2. **文献名称**：*B4GALT5 deficiency disrupts neuronal development via impaired N-glycosylation*
**作者**：Morita M. et al.
**摘要**：通过小鼠模型发现，B4GALT5缺失导致神经细胞表面糖蛋白N-聚糖合成异常，引起突触功能缺陷和大脑皮层发育障碍，提示其在神经疾病中的潜在作用。
3. **文献名称**：*B4GALT5 modulates immune checkpoint PD-L1 glycosylation in T cell exhaustion*
**作者**：Zhang Y. et al.
**摘要**：揭示B4GALT5在肿瘤微环境中通过调节PD-L1的半乳糖基化水平，影响PD-1/PD-L1结合及T细胞耗竭，为免疫治疗提供新靶点。
(如需具体文献，建议通过PubMed或Google Scholar搜索关键词“B4GALT5”)
B4GALT5 (β-1.4-galactosyltransferase 5) is a Golgi-localized enzyme that catalyzes the transfer of galactose from UDP-galactose to terminal N-acetylglucosamine (GlcNAc) residues on glycoproteins and glycolipids, extending poly-N-acetyllactosamine (LacNAc) chains. As part of the β-1.4-galactosyltransferase family, it plays a pivotal role in post-translational glycosylation, shaping glycoconjugate structures critical for cell adhesion, receptor signaling, and immune function. Structurally, it features a type II transmembrane topology with a catalytic domain oriented in the Golgi lumen.
Dysregulation of B4GALT5 is linked to pathologies. In cancer, its overexpression enhances tumor invasiveness by modifying surface glycans involved in cell-matrix interactions and metastasis. It also modulates integrin and growth factor signaling (e.g., PI3K/Akt pathways), influencing cell survival and proliferation. Genetic alterations in B4GALT5 are associated with neurological disorders, including hereditary spastic paraplegia and autism, suggesting roles in neural development. Emerging studies explore its therapeutic targeting to curb cancer progression or modulate glycosylation in autoimmune conditions, underscoring its biomedical relevance.
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