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Recombinant Human FAM129A Protein

  • 中文名: 重组人FAM129A蛋白
  • 别    名: NIBAN1; C1orf24; FAM129A; NIBAN; GIG39; Protein Niban 1; Cell growth-inhibiting gene 39 protein; Protein FAM129A
货号: PA2000-7491
Price: ¥询价
数量:
大包装询价

产品详情

纯度>90%SDS-PAGE.
种属Human
靶点FAM129A
Uniprot NoQ9BZQ8
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-928aa
氨基酸序列MGGSASSQLDEGKCAYIRGKTEAAIKNFSPYYSRQYSVAFCNHVRTEVEQQRDLTSQFLKTKPPLAPGTILYEAELSQFSEDIKKWKERYVVVKNDYAVESYENKEAYQRGAAPKCRILPAGGKVLTSEDEYNLLSDRHFPDPLASSEKENTQPFVVLPKEFPVYLWQPFFRHGYFCFHEAADQKRFSALLSDCVRHLNHDYMKQMTFEAQAFLEAVQFFRQEKGHYGSWEMITGDEIQILSNLVMEELLPTLQTDLLPKMKGKKNDRKRTWLGLLEEAYTLVQHQVSEGLSALKEECRALTKGLEGTIRSDMDQIVNSKNYLIGKIKAMVAQPAEKSCLESVQPFLASILEELMGPVSSGFSEVRVLFEKEVNEVSQNFQTTKDSVQLKEHLDRLMNLPLHSVKMEPCYTKVNLLHERLQDLKSRFRFPHIDLVVQRTQNYMQELMENAVFTFEQLLSPHLQGEASKTAVAIEKVKLRVLKQYDYDSSTIRKKIFQEALVQITLPTVQKALASTCKPELQKYEQFIFADHTNMIHVENVYEEILHQILLDETLKVIKEAAILKKHNLFEDNMALPSESVSSLTDLKPPTGSNQASPARRASAILPGVLGSETLSNEVFQESEEEKQPEVPSSLAKGESLSLPGPSPPPDGTEQVIISRVDDPVVNPVATEDTAGLPGTCSSELEFGGTLEDEEPAQEEPEPITASGSLKALRKLLTASVEVPVDSAPVMEEDTNGESHVPQENEEEEEKEPSQAAAIHPDNCEESEVSEREAQPPCPEAHGEELGGFPEVGSPASPPASGGLTEEPLGPMEGELPGEACTLTAHEGRGGKCTEEGDASQQEGCTLGSDPICLSESQVSEEQEEMGGQSSAAQATASVNAEEIKVARIHECQWVVEDAPNPDVLLSHKDDVKEGEGGQESFPELPSEE
分子量129.5 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.


参考文献

以下是与重组人FAM129A蛋白相关的参考文献示例及其摘要内容(注:文献标题和作者为虚构示例,仅供说明格式):

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1. **文献名称**: *FAM129A regulates ER stress-induced apoptosis via interaction with Bcl-2*

**作者**: Zhang L, et al.

**摘要**: 本研究揭示FAM129A通过结合Bcl-2蛋白调控内质网应激(ER stress)下的细胞凋亡,并成功构建重组人FAM129A蛋白验证其对肿瘤细胞存活的影响。

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2. **文献名称**: *Recombinant FAM129A promotes proliferation and invasion in colorectal cancer cells*

**作者**: Tanaka K, et al.

**摘要**: 利用大肠癌细胞模型,发现重组人FAM129A蛋白通过激活AKT/mTOR信号通路促进肿瘤细胞增殖和迁移,提示其作为潜在治疗靶点的可能性。

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3. **文献名称**: *Expression and functional characterization of recombinant human FAM129A in oxidative stress response*

**作者**: Wang Y, et al.

**摘要**: 首次报道重组人FAM129A蛋白的高效表达与纯化方法,并证实其通过Nrf2通路减轻氧化应激导致的细胞损伤,为相关疾病机制研究提供工具。

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4. **文献名称**: *FAM129A interacts with p53 to modulate DNA damage repair*

**作者**: Gupta S, et al.

**摘要**: 通过重组蛋白结合实验,发现FAM129A与p53直接互作,调控DNA损伤修复过程,在乳腺癌中表现为抑癌基因功能缺失。

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**注意**:以上为基于领域知识的模拟文献,实际研究中建议通过PubMed或Web of Science检索关键词“recombinant FAM129A”或“FAM129A protein function”获取真实文献。


背景信息

Recombinant human FAM129A protein, also known as Niban-like protein 1. is a member of the FAM129 family implicated in cellular stress responses and signaling pathways. Originally identified as a downstream target of the PI3K/AKT/mTOR cascade, FAM129A plays roles in regulating cell survival, proliferation, and apoptosis. Structurally, it contains an N-terminal phosphotyrosine-binding (PTB) domain and conserved C-terminal regions involved in protein interactions. Its expression is upregulated in various cancers, suggesting potential as a biomarker or therapeutic target.

Recombinant forms are typically produced using expression systems like *E. coli* or mammalian cells, enabling functional studies of its post-translational modifications (e.g., phosphorylation) and interactions with partners such as β-catenin or Akt. Research highlights its dual localization (cytoplasmic/nuclear) and context-dependent roles—promoting tumor progression in cancers like melanoma while suppressing oxidative stress in normal cells. Current investigations focus on its mechanistic contributions to diseases, including neurodegeneration and metabolic disorders. Recombinant FAM129A serves as a vital tool for elucidating its physiological and pathological functions, as well as screening modulators for therapeutic development.


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