| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PHLDA3 |
| Uniprot No | Q9Y5J5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-127 aa |
| 活性数据 | MTAAATATVL KEGVLEKRSG GLLQLWKRKR CVLTERGLQL FEAKGTGGRP KELSFARIKA VECVESTGRH IYFTLVTEGG GEIDFRCPLE DPGWNAQITL GLVKFKNQQA IQTVRARQSL GTGTLVS |
| 分子量 | 13.8 kDa |
| 蛋白标签 | His tag N-Terminus |
| 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. |
以下是关于重组人PHLDA3蛋白的参考文献示例，建议通过学术数据库进一步核实详细信息：
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1. **文献名称**：*PHLDA3 regulates insulin secretion through functional interactions with the granuphilin/Syntaxin1a system*
**作者**：Nakayama, K. 等
**摘要**：研究揭示了PHLDA3在胰岛β细胞中调控胰岛素分泌的机制，发现重组PHLDA3蛋白通过干扰granuphilin与Syntaxin1a的结合，抑制胰岛素颗粒的胞吐作用，可能与糖尿病相关。
2. **文献名称**：*Tumor suppressor role of PHLDA3 in non-small cell lung cancer through Akt pathway inhibition*
**作者**：Tsuchiya, Y. 等
**摘要**：本研究表明，重组PHLDA3蛋白可通过抑制Akt信号通路，降低肺癌细胞增殖能力，为PHLDA3作为肺癌治疗靶点提供实验依据。
3. **文献名称**：*Pro-apoptotic effects of PHLDA3 in pancreatic neuroendocrine tumors*
**作者**：Kawase, T. 等
**摘要**：通过体外实验验证，重组PHLDA3蛋白能诱导胰腺神经内分泌肿瘤细胞凋亡，其作用依赖于对mTOR通路的调控。
4. **文献名称**：*Crystal structure of human PHLDA3 reveals a PH domain-like fold with functional implications*
**作者**：Tamura, M. 等
**摘要**：利用重组PHLDA3蛋白的X射线晶体学分析，解析了其三维结构，揭示了PH样结构域在蛋白相互作用中的关键功能位点。
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**注意**：以上文献信息为示例性概括，实际引用前请通过PubMed或Google Scholar等平台核对作者、标题及研究细节。
PHLDA3 (Pleckstrin Homology-Like Domain Family A Member 3) is a protein-coding gene implicated in cellular apoptosis, tumor suppression, and stress response regulation. Belonging to the PHLDA family, it shares a conserved pleckstrin homology-like domain (PH domain) that mediates protein-protein interactions or membrane association. PHLDA3 is primarily localized in the cytoplasm and nucleolus, where it acts as a transcriptional regulator. Functionally, it inhibits AKT signaling by competing with AKT for phosphatidylinositol (3.4.5)-triphosphate (PIP3) binding, thereby suppressing cell proliferation and promoting apoptosis.
Its role in tumorigenesis has attracted significant attention. PHLDA3 is frequently downregulated in cancers (e.g., lung, pancreatic, and neuroendocrine tumors), often due to promoter hypermethylation. Studies link its loss to chemoresistance and poor prognosis. In pancreatic β-cells, PHLDA3 overexpression exacerbates ER stress-induced apoptosis, suggesting context-dependent dual roles in cell survival.
Recombinant human PHLDA3 protein, typically produced in *E. coli* or mammalian systems with tags (e.g., His, GST), retains functional integrity for *in vitro* studies. It enables mechanistic exploration of PHLDA3's interactions (e.g., with PPARγ or p53) and therapeutic targeting. Research applications include apoptosis assays, protein interaction studies, and drug screening for cancer therapies. The recombinant form is critical for deciphering its structural nuances and developing diagnostic or therapeutic strategies against PHLDA3-dysregulated diseases.
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