Anti-Insulin Receptor/INSR Antibody Picoband®

Overview

Anti-Insulin Receptor/INSR Antibody Picoband® is an antibody targeting INSR. Common applications include WB, IHC, Flow Cytometry, ELISA. Key specifications include host: Rabbit; clonality: Polyclonal; isotype: Rabbit IgG; reactivity: Human,Mouse,Rat; observed MW: 155 kDa; calculated MW: 156333 MW.

Boster Bio Anti-Insulin Receptor/INSR Antibody catalog # PA1620. Tested in WB applications. This antibody reacts with Human, Mouse, Rat. The brand Picoband indicates this is a premium antibody that guarantees superior quality, high affinity, and strong signals with minimal background in Western blot applications. Only our best-performing antibodies are designated as Picoband, ensuring unmatched performance.

Key elements and design rationale

• Target: INSR — Insulin receptor
• Antibody format: Host: Rabbit; Clonality: Polyclonal; Isotype: Rabbit IgG
• Species reactivity: Human,Mouse,Rat
• Molecular weight guidance: Observed: 155 kDa; Calculated: 156333 MW

Specificity note: No cross reactivity with other proteins.

Biological background

Protein function (datasheet): 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 phosphotyrosines 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. PubMed:12138094 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, PubMed:16831875 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. .

Scientific background (datasheet): INSR (INSULIN RECEPTOR) is a tetramer of 2 alpha and 2 beta subunits that are coded by a single gene and are joined by disulfide bonds, a mechanism parallel to that of its ligand, insulin. It belongs to the large class of tyrosine kinase receptors. The insulin receptor gene is mapped to 19p13.2. The insulin receptor mediates their activity by causing the addition of a phosphate group to particular tyrosines on certain proteins within a cell. The INSR gene spans more than 120 kb and has 22 exons. Functional studies of the INSR SNPs show no effect on mRNA levels or splicing in peripheral blood leukocytes or on binding of insulin to mononuclear cells.

Cellular localization (datasheet): Cell membrane; Single-pass type I membrane protein.

Tissue details (datasheet): Isoform Long and isoform Short are predominantly expressed in tissue targets of insulin metabolic effects: liver, adipose tissue and skeletal muscle but are also expressed in the peripheral nerve, kidney, pulmonary alveoli, pancreatic acini, placenta vascular endothelium, fibroblasts, monocytes, granulocytes, erythrocytes and skin. Isoform Short is preferentially expressed in fetal cells such as fetal fibroblasts, muscle, liver and kidney. Found as a hybrid receptor with IGF1R in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen and placenta (at protein level). Overexpressed in several tumors, including breast, colon, lung, ovary, and thyroid carcinomas. .

Sequence similarities (datasheet): Belongs to the protein kinase superfamily. Tyr protein kinase family. Insulin receptor subfamily.

Research relevance and current trends

• Commonly studied in contexts related to Adapters,Cancer,Cytoplasmic,Neuroscience,Neurotransmission,Protein Phosphorylation,Receptor Tyrosine Kinases,Receptors / Channels,Signal Transduction,Tyrosine Kinases.
• Supports comparative expression analysis across conditions, genotypes, or treatments when paired with appropriate controls.
• Useful for confirming target presence and subcellular distribution using orthogonal readouts (e.g., microscopy vs. immunoblotting).

Common research applications

• Western blot (WB): Compare relative target abundance and apparent size/isoforms across samples; interpret bands in light of expected MW and potential PTMs.
• ELISA: Measure target abundance in compatible matrices using a standard-curve readout; ensure dilution linearity and appropriate controls.
• Immunohistochemistry (IHC): Assess tissue distribution and cell-type patterns; interpret staining with appropriate negative controls and antigen context.
• Flow cytometry: Quantify target-positive populations in single-cell suspensions; pair with viability and isotype/FMO controls conceptually.

Notes for experimental interpretation

• Consider isoforms, post-translational modifications, and processing that can shift apparent molecular weight or localization.
• Cross-reactivity (datasheet): No cross-reactivity with other proteins
• Use appropriate positive and negative controls (e.g., KO/KD, blocking peptide, or isotype controls) to support specificity interpretation.

As a polyclonal antibody, this reagent may recognize multiple epitopes on the target, which can improve detection robustness but may require careful specificity controls.

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.