Insulin Receptor β (Phospho Tyr1345) rabbit pAb
活动价:
市场价:¥880.00
- 50μL
- 100μL
FAB2612129
- 产品信息
商品描述
靶点-Target
Insulin R
反应性
Human,Rat,Mouse,
应用
WB
宿主物种-Host Species
Rabbit
同种型-Isotype
IgG
修饰-Modification
Phospho
MW(Observed)
95kD
推荐稀释比
WB 1:1000-2000
组成
Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
纯化工艺
The antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
储存
-15°C to -25°C/1 year(Do not lower than -25°C)
浓度
1 mg/ml
克隆性
Polyclonal
免疫原
Synthesized phosho peptide around human Insulin Receptor β (Tyr1345)
特异性
This antibody detects endogenous levels of Human Insulin Receptor β (phospho-Tyr1345)
基因名称
INSR
蛋白名称
Insulin Receptor β (Tyr1345)
别名
Insulin receptor;IR;CD antigen CD220;[Cleaved into: Insulin receptor subunit alpha;Insulin receptor subunit beta]
Organism-1
Human
基因ID-1
3643
SwissProt-1
P06213
Organism-2
Mouse
基因ID-2
16337
SwissProt-2
P15208
Organism-3
Rat
SwissProt-3
P15127
背景
This gene encodes a member of the receptor tyrosine kinase family of proteins. The encoded preproprotein is proteolytically processed to generate alpha and beta subunits that form a heterotetrameric receptor. Binding of insulin or other ligands to this receptor activates the insulin signaling pathway, which regulates glucose uptake and release, as well as the synthesis and storage of carbohydrates, lipids and protein. Mutations in this gene underlie the inherited severe insulin resistance syndromes including type A insulin resistance syndrome, Donohue syndrome and Rabson-Mendenhall syndrome. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2015],
细胞定位
Cell membrane ; Single-pass type I membrane protein . Late endosome . Lysosome . Binding of insulin to INSR induces internalization and lysosomal degradation of the receptor, a means for down-regulating this signaling pathway after stimulation. In the presence of SORL1, internalized INSR molecules are redirected back to the cell surface, thereby preventing their lysosomal catabolism and strengthening insulin signal reception. .





