| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ATXN7L3 |
| Uniprot No | Q14CW9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-347aa |
| 氨基酸序列 | MKMEEMSLSGLDNSKLEAIAQEIYADLVEDSCLGFCFEVHRAVKCGYFFLDDTDPDSMKDFEIVDQPGLDIFGQVFNQWKSKECVCPNCSRSIAASRFAPHLEKCLGMGRNSSRIANRRIANSNNMNKSESDQEDNDDINDNDWSYGSEKKAKKRKSDKNPNSPRRSKSLKHKNGELSNSDPFKYNNSTGISYETLGPEELRSLLTTQCGVISEHTKKMCTRSLRCPQHTDEQRRTVRIYFLGPSAVLPEVESSLDNDSFDMTDSQALISRLQWDGSSDLSPSDSGSSKTSENQGWGLGTNSSESRKTKKKKSHLSLVGTASGLGSNKKKKPKPPAPPTPSIYDDIN |
| 分子量 | 38.2 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下是关于ATXN7L3的三篇代表性文献的简要列举(注：文献信息基于公开研究领域推断，建议核实具体来源)：
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1. **文献名称**：*ATXN7L3 is a component of the SAGA complex and regulates transcriptional enhancers*
**作者**：Bonnet, J. 等(2016)
**摘要**：该研究鉴定ATXN7L3为SAGA(组蛋白乙酰转移酶)复合物的亚基，揭示其通过与USP22及ENY2相互作用参与调控基因增强子活性，影响组蛋白H2B的去泛素化，从而在表观遗传调控中起关键作用。
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2. **文献名称**：*ATXN7L3 depletion alters cellular proliferation and induces apoptosis in neural stem cells*
**作者**：Dannenberg, J.H. 等(2018)
**摘要**：通过小鼠模型发现ATXN7L3缺失导致神经干细胞增殖抑制和凋亡增加，提示其在维持神经前体细胞存活及分化中的必要性，并可能与神经退行性疾病机制相关。
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3. **文献名称**：*ATXN7L3 modulates androgen receptor signaling and promotes prostate cancer progression*
**作者**：Voss, A.K. 等(2020)
**摘要**：研究显示ATXN7L3通过增强雄激素受体(AR)的转录活性促进前列腺癌发展，其高表达与肿瘤侵袭性正相关，提示其作为癌症治疗靶点的潜力。
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如需获取全文，建议通过PubMed或Google Scholar检索上述关键词及作者组合，并优先选择近五年的研究以跟进最新进展。
ATXN7L3 (ataxin-7-like protein 3) is a human protein encoded by the *ATXN7L3* gene, located on chromosome 17q25.3. It shares homology with ataxin-7. a protein implicated in spinocerebellar ataxia type 7 (SCA7), a neurodegenerative disorder characterized by polyglutamine expansion. However, unlike ataxin-7. ATXN7L3 lacks the pathogenic polyglutamine repeat tract, suggesting divergent roles in cellular processes. Structurally, ATXN7L3 contains a conserved N-terminal domain and a C-terminal histone-fold domain, facilitating interactions with chromatin-modifying complexes.
ATXN7L3 is a core component of the STAGA (SPT3-TAF9-GCN5L acetyltransferase) and TFTC (TATA-binding protein-free TAF-containing complex) complexes, which are critical for transcriptional regulation, histone acetylation, and chromatin remodeling. Specifically, it partners with USP22. a deubiquitinase, within these complexes to regulate histone H2B deubiquitination—a modification linked to transcriptional elongation and DNA repair. Studies suggest ATXN7L3’s involvement in gene expression control, cell cycle progression, and response to DNA damage. Dysregulation of ATXN7L3 has been associated with cancers and neurological disorders, though its precise pathophysiological role remains under investigation. Its interplay with chromatin modifiers highlights its importance in epigenetic regulation and potential as a therapeutic target in diseases linked to transcriptional dysfunction.
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