活性:通过其结合荧光素偶联的大肠杆菌生物颗粒的能力来衡量。ED50使用His Tag Antibody包被板的这种效果为0.15-0.9μg/mL
来源:小鼠骨髓瘤细胞系,NS0 衍生的人 TREM-2 蛋白
Accession#:Q9NZC2
N-端序列:His19
预测分子量:18 kDa
SDS-PAGE:25-39 kDa,还原条件
形式:从0.2 µm过滤的HEPES和NaCl溶液中冻干。
复溶:在水中以500 μg/mL重新配制。
运输:产品在环境温度下运输。收到后,立即将其存放在下文建议的温度下。
储存/稳定性:避免重复冻融循环。复溶后,在无菌条件下2至8℃,1个月;-20至-70℃,3个月。
货号
产品名称
规格
9256-T2-050
Recombinant Human TREM2 His-tag Protein, CF
50 µg
TREM-2 (Triggering Receptor Expressed on Myeloid cells-2) is a 35 kDa type I transmembrane member of the TREM family and Ig superfamily (1). Mature human TREM-2 consists of a 156 amino acid (aa) extracellular domain (ECD) with one V-type Ig-like domain, a 21 aa transmembrane (TM) domain, and a 35 aa cytoplasmic tail (2). Within the ECD, human TREM-2 shares 73% and 74% aa sequence identity with mouse and rat TREM-2, respectively. Soluble forms of the TREM-2 ECD are generated by alternative splicing or proteolytic cleavage, and the cytoplasmic domain can be liberated by gamma-Secretase mediated intramembrane cleavage (3). A positively charged lysine within the transmembrane segment allows association with the signal adapter protein, DAP12 and inhibition of macrophage activation (4, 5). TREM-2 is expressed on macrophages, immature myeloid dendritic cells, osteoclasts, microglia, and adipocytes (5-9). It promotes the differentiation and function of osteoclasts, the production of inflammatory cytokines by adipocytes, insulin resistance, and the phagocytic clearance of bacteria (9-11). In the CNS, TREM-2 binds to ApoE, ApoA1, and ApoB and mediates the clearance of apoptotic neurons, amyloid plaques, and cell debris following demyelination (6-8, 12). TREM-2 also interacts with and modifies signaling through Plexin A1 on dendritic cells and osteoclasts (13). Mutations in TREM-2 or DAP12 are associated with the development of Alzheimer's disease and Nasu-Hakola disease (NHD/PLOSL) which is characterized by presenile dementia and bone cysts (14, 15). Soluble TREM-2 is elevated in cerebrospinal fluid of patients with active multiple sclerosis (MS), and TREM-2 blockade exacerbates disease symptoms in the experimental EAE model of MS (16, 17).
Selective Eradication of Colon Cancer Cells Harboring PI3K and/or MAPK Pathway Mutations in 3D Culture by Combined PI3K/AKT/mTOR Pathway and MEK Inhibition Authors: VS Atanasova, A Riedl, M Strobl, J Flandorfer, D Unterleuth, C Weindorfer, P Neuhold, S Stang, M Hengstschl, M Bergmann, H Dolznig International Journal of Molecular Sciences, 2023;24(2):.