
- SynonymGPNMB,HGFIN,NMB,Osteoactivin
- SourceHuman Osteoactivin, His Tag (GPB-H5229) is expressed from human 293 cells (HEK293). It contains AA Ala 22 - Pro 486 (Accession # AAH32783).Predicted N-terminus: Ala 22Request for sequence
- Molecular Characterization
This protein carries a polyhistidine tag at the C-terminus.
The protein has a calculated MW of 53.4 kDa. The protein migrates as 85-100 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
- EndotoxinLess than 1.0 EU per μg by the LAL method.
- Purity
>95% as determined by SDS-PAGE.
- Formulation
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
Contact us for customized product form or formulation.
- Reconstitution
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
- Storage
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
- -20°C to -70°C for 12 months in lyophilized state;
- -70°C for 3 months under sterile conditions after reconstitution.

Human Osteoactivin, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
- Citations
Osteoactivin regulates head and neck squamous cell carcinoma invasion by modulating matrix metalloproteases
Authors: Arosarena OA, et al.
Journal: J Cell Physiol 2017
Application: Cell culture
Request for Full-text
- BackgroundTransmembrane glycoprotein NMB (GPNMB) is also known as Transmembrane glycoprotein HGFIN, DC-HIL and Osteoactivin (OA), which belongs to the PMEL/NMB family. GPNMB contains one PKD domain. GPNMB is a transmembrane glycoprotein that is up-regulated in various cancer cells, including in glioblastoma multiforme and is expressed in many melanoma cells, as well as in tissue macrophages. GPNMB protein acts as a downstream mediator of BMP-2 effects on osteoblast differentiation and function. GPNMB participates in bone mineralization, and functions as a negative regulator of inflammation in macrophages.
- References
- (1)Weterman MA., et al., 1995, International Journal of Cancer 60 (1): 73–81.
- (2)Abdelmagid, SM., et al., 2008, Exp Cell Res 314 (13): 2334–51.
- (3)Abdelmagid SM., et al., 2007, J Cell Physiol. 210 (1): 26–37.
Please contact us via TechSupport@acrobiosystems.com if you have any question on this product.
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1-s2.0-S016816561001878X-main.pdf(521.01k)
缓慢的代谢在许多重要的方面保护了白血病细胞,使得它们能够更好的生存。研究小组还发现了一种针对这一独特代谢状态的实验性药物,并已开始检测它治疗这一疾病的效力。研究人员将相关结果发表在1月17日的《细胞干细胞》(CellStemCell)杂志上。
研究的通讯作者、罗彻斯特大学医学中心癌症中心教授CraigT.Jordan博士正在与一个药物制造商建立合作关系,在这一领域开展进一步的测试。实验室研究中的化合物已被用于临床试验。
Jordan说:“我们认为针对白血病干细胞代谢是一种独特的方法,有潜力广泛应用于几种形式的白血病。我们的研究工作令人感到兴奋,是因为我们鉴别出了一些现正开发用于临床的药物,我们希望其有巨大的潜力,可很快用于改善白血病患者的护理。”
主要研究员、Jordan实验室博士后EleniLagADInou说,当研究小组发现白血病干细胞的代谢与其他的肿瘤细胞如此不同之时,他们集中研究了这一过程的确切作用机制。
他们发现,白血病干细胞是通过一种称作氧化磷酸化的单一过程,在线粒体中生成了它们需要的所有能量。相比之下,其他的癌细胞和正常干细胞还依赖于第二种燃料来源——糖酵解来生成能量。
获得了这一新信息,随后研究人员探索了与氧化磷酸化相关的信号通路,以寻找致命弱点终止这一过程。他们发现一种称作BCL-2的重要基因表达增高,这对于白血病干细胞能量生成至关重要。
研究小组还了解了制药行业处于不同研发阶段的BCL-2抑制药物;Lagadinou和Jordan发现了两种这样的化合物,并在人类白血病样本中对它们进行了测试。研究结果表明,药物倾向性杀死不活跃的、代谢较慢的白血病干细胞。
众所周知,白血病细胞能够长时间休眠,在接受治疗后,可以突然发动另一轮的攻击。
Lagadinou说:“这种治疗有望靶向传统药物相对无法触及的,休眠白血病干细胞亚群。还有重要的一点需要指出,化合物不会损伤正常细胞,因为正常细胞能力利用另一条信号通路来生成能量。”
不会对健康细胞产生毒性,研究人员希望这些药物能够在缓解期靶向这一疾病,此时肃清残余白血病是极其重要的。
白血病,这种血癌可分为四种常见类型:急性髓系白血病(AML)、急性淋巴细胞白血病(ALL)、慢性粒细胞白血病(CML)和慢性淋巴细胞白血病(CLL)。AML在成人中最常见,且最难治疗,其部分原因是它影响了未成熟细胞。每年近5万新病例被确诊,约一半人死亡。
研究人员发现在过去的十年里,许多治疗并非旨在除去白血病根源——“白血病干细胞”,因此从未真正根除这一疾病。
Jordan说,事实上,即便是最现代的癌症治疗也是假设:所有的癌症代谢都依赖于糖酵解作为燃料来源。新研究发现氧化磷酸化是白血病干细胞的唯一燃料来源,这对提出新的改进治疗具有格外的意义(本文来自生物谷)
更多关于细胞学文章:http://www.hbzhan.com/st100044
希望能帮到你。
酶的作用是催化剂,促进或抑制反应的进行.加热主要是通过升高温度加快反应速率,无机催化剂和酶的原理相同,都是通过降低反应的活化能加快反应速率

