生物来源
rabbit
质量水平
偶联物
unconjugated
抗体形式
affinity isolated antibody
抗体产品类型
primary antibodies
克隆
polyclonal
表单
buffered aqueous solution
分子量
antigen ~57 kDa by calculation
种属反应性
human
技术
western blot: 1:500-1:1,000
UniProt登记号
运输
dry ice
储存温度
−20°C
基因信息
human ... SLC2A10(81031)
免疫原
peptide corresponding to the human GLUT10 protein (amino acids 367-385).
生化/生理作用
GLUT10 is a glucose transporter that is encoded by the gene SLC2A10, and is highly expressed in liver and pancreas. Polymorphisms in SLC2A10 may not influence the pathogenesis of type 2 diabetes but the expression of GLUT10 and the interaction with TGF-β signaling pathway has important role in the development of peripheral arterial disease in patients with type 2 diabetes. GLUT10 is also required for the development of cardiovascular system and the notochord in zebrafish embryos.
外形
Solution of 1 mg/mL in phosphate buffered saline containing 0.02% sodium azide.
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储存分类代码
10 - Combustible liquids
WGK
nwg
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Gitte Andersen et al.
Diabetes, 52(9), 2445-2448 (2003-08-28)
The SLC2A10 gene encodes the GLUT10 facilitative glucose transporter, which is expressed in high amounts in liver and pancreas. The gene is mapped to chromosome 20q12-q13.1, a region that has been shown to be linked to type 2 diabetes. The
Andy Willaert et al.
Human molecular genetics, 21(6), 1248-1259 (2011-11-26)
Growth factor signaling results in dramatic phenotypic changes in cells, which require commensurate alterations in cellular metabolism. Mutations in SLC2A10/GLUT10, a member of the facilitative glucose transporter family, are associated with altered transforming growth factor-β (TGFβ) signaling in patients with
Yi-Der Jiang et al.
BMC medical genetics, 11, 126-126 (2010-08-26)
Recent data indicate that loss-of-function mutation in the gene encoding the facilitative glucose transporter GLUT10 (SLC2A10) causes arterial tortuosity syndrome via upregulation of the TGF-β pathway in the arterial wall, a mechanism possibly causing vascular changes in diabetes. We genotyped
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