Recombinant Mouse TMEM106B Protein
Beta LifeScience
SKU/CAT #: BLK-01316P-100UG

Mouse TMEM106B on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.
Recombinant Mouse TMEM106B Protein
Beta LifeScience
SKU/CAT #: BLK-01316P-100UG
Collections: High-quality recombinant proteins, Other recombinant proteins
Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.
Product Overview
Description | Recombinant Mouse TMEM106B Protein is expressed from HEK293 with hFc tag at the C-Terminus.It contains Pro119-Gln275. |
Purity | > 95% as determined by Tris-Bis PAGE;> 95% as determined by HPLC |
Accession | Q80X71 |
Target Symbol | TMEM106B |
Synonyms | Transmembrane protein 106B;Tmem106b |
Species | Mouse |
Expression System | HEK293 |
Tag | C-hFc |
Expression Range | Pro119-Gln275 |
Mol. Weight | The protein has a predicted MW of 44.8 kDa. Due to glycosylation, the protein migrates to 65-68 kDa based on Tris-Bis PAGE result. |
Form | Lyophilized |
Formulation | Lyophilized from 0.22um filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization. |
Endotoxin | Less than 1EU per ug by the LAL method. |
Storage | Reconstituted protein stable at -80°C for 12 months, 4°C for 1 week. Use a manual defrost freezer and avoid repeated freeze-thaw cycles. |
Shipping | Shipped at ambient temperature. |
Gene Background | TMEM106B is a well-recognised risk factor for FTD caused by GRN mutation. Elegant experiments have suggested that increased risk for FTD is due to elevated levels of TMEM106B (Nicholson et al, 2013; Gallagher et al, 2017). Therefore, recent work has explored the therapeutic potential of reducing TMEM106B levels, with initial results looking encouraging, as crossing a Grn-deficient mouse to a Tmem106b knockout showed a rescue in FTD-related behavioural defects and specific aspects of lysosome dysfunction (Klein et al, 2017). |