Recombinant Human INSR Protein (M1-S1382), eGFP, Strep II, 10×His tagged

• Cat.No.: INSR-0997H
• Product Overview: Recombinant Human IR(M1-S1382 end) (Y999F, S1001A, D1159N, R1372A, I1373A, L1374A, L1376A)-3C-eGFP-Strep II-10His Protein was expressed in Mammalian cell.

Specification

• Description: 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 pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport. Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD; regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway. The Ras/RAF/MAP2K/MAPK pathway is mainly involved in mediating cell growth, survival and cellular differentiation of insulin. Phosphorylated IRS1 recruits GRB2/SOS complex, which triggers the activation of the Ras/RAF/MAP2K/MAPK pathway. In addition to binding insulin, the insulin receptor can bind insulin-like growth factors (IGFI and IGFII). Isoform Short has a higher affinity for IGFII binding. When present in a hybrid receptor with IGF1R, binds IGF1. shows that hybrid receptors composed of IGF1R and INSR isoform Long are activated with a high affinity by IGF1, with low affinity by IGF2 and not significantly activated by insulin, and that hybrid receptors composed of IGF1R and INSR isoform Short are activated by IGF1, IGF2 and insulin. In contrast, shows that hybrid receptors composed of IGF1R and INSR isoform Long and hybrid receptors composed of IGF1R and INSR isoform Short have similar binding characteristics, both bind IGF1 and have a low affinity for insulin. In adipocytes, inhibits lipolysis.
• Source: Mammalian cell
• Species: Human
• Tag: His&StrepII&EGFP
• Form: Liquid
• Protein length: M1-S1382
• Endotoxin: < 0.01 EU per μg of the protein
• Purity: 80%
• Stability: Samples are stable for up to twelve months from date of receipt at -20 to -80 centigrade.
• Storage: Store it under sterile conditions at -20 to -80 centigrade. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Storage Buffer: 50 mM Tris-HCl (pH7.5), 200 mM NaCl, 20% glycerol
  Supplied as sterile 20 mM HEPES pH 7.5, 150 mM NaCl, 0.02% (w/v) DDM, 0.002% (w/v) CHS
• Shipping: It is shipped out with blue ice.

Gene Information

• Gene Name: INSR insulin receptor [ Homo sapiens (human) ]
• Official Symbol: INSR
• Synonyms: INSR; insulin receptor; CD220; IR; HHF5
• Gene ID: 3643
• mRNA Refseq: NM_000208
• Protein Refseq: NP_000199
• MIM: 147670
• UniProt ID: P06213

Reviews

02/25/2020

The compatibility with a range of lab equipment streamlined experimental procedures, saving both time and effort.

04/26/2016

The product's support in the form of educational resources positively impacted the learning curve for our researchers.

04/18/2016

The proactive engagement with customer insights contributed to the product's ongoing relevance in the scientific community.

Q&As

What impact does malfunction or dysregulation of the insulin receptor (INSR) have on metabolic health?

Malfunction or dysregulation of the insulin receptor (INSR) can lead to disturbances in metabolic health, contributing to conditions like diabetes.

How does the insulin receptor (INSR) function in regulating glucose metabolism in cells?

INSR regulates glucose metabolism by facilitating the cellular uptake of glucose in response to insulin.

What are the key tissues or cell types where the insulin receptor (INSR) is prominently expressed?

The insulin receptor (INSR) is prominently expressed in tissues such as the liver, muscle, and adipose tissue.

Are there known genetic variations or mutations in the insulin receptor (INSR) associated with metabolic disorders or insulin resistance?

Genetic variations or mutations in the insulin receptor (INSR) are associated with certain metabolic disorders and insulin resistance.

In the context of diabetes, what role does the insulin receptor (INSR) play in the development of insulin resistance?

In diabetes, the insulin receptor (INSR) contributes to the development of insulin resistance, impairing its normal signaling functions.

What is the primary role of the insulin receptor (INSR) protein in cellular processes?

The insulin receptor (INSR) protein plays a crucial role in cellular processes, particularly in mediating the effects of insulin.

How does the insulin receptor (INSR) activate downstream signaling pathways in response to insulin binding?

Upon insulin binding, the insulin receptor (INSR) activates downstream signaling pathways, including the PI3K-AKT pathway.