Insulin / IGF Signaling Antibody Sampler Pack

Insulin / IGF Signaling Antibody Sampler Pack

The Insulin / IGF Signaling Antibody Sampler Pack from Assay Genie brings together 8 rigorously validated antibodies spanning the key nodes of this pathway, supplied in a convenient 20µL trial size. It lets researchers screen an entire signalling axis in a single, cost-effective pack — validated for applications including ELISA, IF/ICC, IHC-P, IP, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

Insulin and insulin-like growth factor signaling coordinates nutrient uptake, anabolic metabolism, growth, and survival, and its dysregulation lies at the heart of type 2 diabetes, metabolic syndrome, and cancer. The cascade begins when insulin engages the Insulin Receptor, a ligand-activated receptor tyrosine kinase that autophosphorylates and recruits scaffolding adaptors, chiefly IRS-1, which becomes tyrosine phosphorylated to create docking sites for class IA PI3-kinase. The lipid products of PI3K activate the serine/threonine kinase AKT, whose full activation is reflected by phosphorylation at serine 473; monitoring AKT (pan) together with Phospho-AKT S473 distinguishes total enzyme from its active fraction. Activated AKT orchestrates the metabolic actions of insulin through several effectors. It phosphorylates and inhibits GSK-3beta, relieving the inhibition of Glycogen Synthase to promote glycogen storage. It drives translocation of the glucose transporter GLUT4/SLC2A4 to the plasma membrane, accelerating glucose uptake in muscle and adipose tissue. AKT also phosphorylates the transcription factor FoxO1, triggering its nuclear exclusion and thereby suppressing gluconeogenic and catabolic gene programs. Closely related IGF receptors share these adaptors and converge on the same PI3K-AKT module, extending the same logic from metabolic control to organismal growth. In states of insulin resistance, impaired IRS-1 signaling and blunted AKT activation lead to reduced GLUT4 mobilization, diminished glycogen synthesis, and unrestrained FoxO1-driven hepatic glucose output, while in cancer the same axis is frequently hyperactivated to sustain proliferation. Profiling the Insulin Receptor, IRS-1, AKT and its serine 473 phosphorylation, GSK-3beta, GLUT4/SLC2A4, FoxO1, and Glycogen Synthase together captures the flow of information from receptor to metabolic endpoint. This pack brings together validated antibodies against these key targets to support comprehensive investigation of insulin and IGF signaling.