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Recombinant Human ATAD3B Protein

  • 中文名: 重组人ATP酶家族AAA结构域包含蛋白3B(ATAD3B)
  • 别    名: ATAD3B; KIAA1273; TOB3; ATPase family AAA domain-containing Protein 3B; AAA-TOB3
货号: PA2000-5670
Price: ¥询价
数量:
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点ATAD3B
Uniprot NoQ5T9A4
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-648aa
氨基酸序列MSWLFGVNKGPKGEGAGPPPPLPPAQPGAEGGGDRGLGDRPAPKDKWSNFDPTGLERAAKAARELEHSRYAKEALNLAQMQEQTLQLEQQSKLKEYEAAVEQLKSEQIRAQAEERRKTLSEETRQHQARAQYQDKLARQRYEDQLKQQRLLNEENLRKQEESVQKQEAMRRATVEREMELRHKNEMLRVETEARARAKAERENADIIREQIRLKASEHRQTVLESIRTAGTLFGEGFRAFVTDRDKVTATVAGLTLLAVGVYSAKNATAVTGRFIEARLGKPSLVRETSRITVLEALRHPIQVSRRLLSRPQDVLEGVVLSPSLEARVRDIAIATRNTKKNRGLYRHILLYGPPGTGKTLFAKKLALHSGMDYAIMTGGDVAPMGREGVTAMHKLFDWANTSRRGLLLFMDEADAFLRKRATEEISKDLRATLNAFLYHMGQHSNKFMLVLASNLPEQFDCAINSRIDVMVHFDLPQQEERERLVRLHFDNCVLKPATEGKRRLKLAQFDYGRKCSEVARLTEGMSGREIAQLAVSWQATAYASKDGVLTEAMMDACVQDAVQQYRQKMRWLKAEGPGRGVEHPLSGVQGETLTSWSLATDPSYPCLAGPCTFRICSWMGTGLCPGPLSPRMSCGGGRPFCPPGHPLL
分子量99 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.


参考文献

以下是关于重组人ATP酶家族AAA结构域包含蛋白3B(ATAD3B)的3篇代表性文献的简要信息:

1. **文献名称**: *ATAD3B is a negative regulator of mitochondrial DNA release and colorectal cancer progression*

**作者**: Zhong Y, et al.

**摘要**: 研究发现ATAD3B在结直肠癌中表达下调,其缺失导致线粒体DNA异常释放,激活cGAS-STING通路,促进肿瘤细胞迁移和侵袭,提示其作为肿瘤抑制因子的潜在作用。

2. **文献名称**: *ATAD3B and ATAD3A synergistically maintain mitochondrial DNA stability through cooperative interaction with mitochondrial nucleoids*

**作者**: He J, et al.

**摘要**: 研究揭示了ATAD3B与同源蛋白ATAD3A共同调控线粒体DNA(mtDNA)的稳定性,二者通过与线粒体核苷酸复合物相互作用维持mtDNA结构和复制功能,影响细胞能量代谢稳态。

3. **文献名称**: *ATAD3B promotes neuroblastoma cell proliferation by interacting with MYCN to regulate mitochondrial dynamics*

**作者**: Meng Q, et al.

**摘要**: ATAD3B在神经母细胞瘤中高表达,与MYCN癌蛋白协同调控线粒体动态(融合/分裂),增强线粒体呼吸和细胞增殖,提示其作为潜在治疗靶点。

4. **文献名称**: *The AAA+ protein ATAD3B is a novel binding partner of the mitochondrial protein SAMM50 and modulates cristae structure*

**作者**: Gilquin B, et al.

**摘要**: 该研究通过蛋白质互作分析,发现ATAD3B在线粒体嵴形态调控中与SAMM50蛋白协同作用,影响呼吸链复合体组装和氧化磷酸化效率,为线粒体功能障碍相关疾病提供机制线索。

这些研究涵盖了ATAD3B在癌症、线粒体功能和细胞代谢等领域的分子机制探索。如需具体文献来源,建议通过PubMed或SciHub输入标题或作者检索全文。


背景信息

ATAD3B (ATPase family AAA domain-containing protein 3B) is a mitochondrial protein encoded by the nuclear genome, belonging to the AAA+ ATPase superfamily. It shares structural homology with ATAD3A, its paralog, including an N-terminal transmembrane domain anchoring it to the mitochondrial inner membrane and a C-terminal AAA+ ATPase domain critical for energy-dependent protein interactions. ATAD3B is evolutionarily conserved and predominantly expressed in tissues with high metabolic demands, such as the brain, heart, and skeletal muscle.

Functionally, ATAD3B is implicated in mitochondrial dynamics, cholesterol metabolism, and mitochondrial DNA (mtDNA) organization. Unlike ATAD3A, which is essential for mitochondrial biogenesis and cell viability, ATAD3B may act as a regulatory modifier or compensatory factor. Studies suggest it modulates ATAD3A activity, potentially influencing mitochondrial respiratory chain assembly and membrane integrity. Dysregulation of ATAD3B is associated with neurodevelopmental disorders, cancer progression, and mitochondrial encephalopathies. For instance, reduced ATAD3B expression correlates with altered mitochondrial cristae morphology and impaired oxidative phosphorylation.

Recent research highlights its role in tumor suppression, where epigenetic silencing of ATAD3B in certain cancers promotes metabolic reprogramming and chemoresistance. However, its exact molecular mechanisms and interactions with mitochondrial nucleoid components remain under investigation, offering avenues for understanding mitochondrial dysfunction-related pathologies.


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