The Mouse Insulin Receptor (INSR) ELISA Kit is a powerful tool for measuring insulin receptor levels in mouse serum, plasma, and cell culture supernatants. This kit provides accurate and reliable results with high sensitivity and specificity, making it ideal for various research applications.The insulin receptor is a key protein involved in regulating glucose metabolism and is essential for maintaining proper blood sugar levels. Dysregulation of the insulin receptor is linked to conditions such as diabetes, obesity, and metabolic syndrome, making it a valuable biomarker for studying these conditions and developing potential treatments.
With its easy-to-use format and robust performance, the Mouse INSR ELISA Kit is a valuable asset for researchers studying insulin signaling pathways and investigating potential therapeutic interventions for metabolic disorders.
Product Name:
Mouse Insulin receptor (Insr) ELISA Kit
SKU:
MOEB0657
Size:
96T
Target:
Mouse Insulin receptor (Insr)
Synonyms:
CD220, IR
Assay Type:
Sandwich
Detection Method:
ELISA
Reactivity:
Mouse
Detection Range:
0.312-20ng/mL
Sensitivity:
0.158ng/mL
Intra CV:
4.2%
Inter CV:
7.4%
Linearity:
Sample
1:2
1:4
1:8
1:16
Serum(N=5)
105-115%
96-106%
111-120%
92-102%
EDTA Plasma(N=5)
103-116%
99-109%
110-120%
111-111%
Heparin Plasma(N=5)
108-119%
105-114%
83-95%
95-105%
Recovery:
Sample Type
Average(%)
Recovery Range(%)
Serum
95
89-101
Plasma
97
91-103
Function:
Receptor tyrosine kinase which mediates the pleiotropic actions of insulin. Binding of insulin leads to phosphorylation of several intracellular substrates, including, insulin receptor substrates (IRS1, 2, 3, 4), SHC, GAB1, CBL and other signaling intermediates. Each of these phosphorylated proteins serve as docking proteins for other signaling proteins that contain Src-homology-2 domains (SH2 domain) that specifically recognize different phosphotyrosine residues, including the p85 regulatory subunit of PI3K and SHP2. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK