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Mutations in the receptor gene cause the inherited resistant syndromes Leprechaunism and Rabson–Mendenhall syndrome. These recessive conditions are characterized by intrauterine and post-natal growth restrictions, dysmorphic features, altered glucose homeostasis, and early demise.

The large docking protein IRS-1 is a major substrate for the receptor and other tyrosine kinases. It plays a key role in eliciting many of 's actions, including binding and activation of phosphatidylinositol (PI) 3-kinase and the subsequent increase in glucose transport.

IRS1 in the liver is more important for signaling in the late refeeding period, whereas IRS2 signaling is mostly dominating in the period directly after food intake and during fasting.

The causes of type 1 diabetes are unknown, although several risk factors have been identified. The risk of developing type 1 diabetes is increased by certain variants of the HLA-DQA1, HLA-DQB1, and HLA-DRB1 genes. These genes provide instructions for making proteins that play a critical role in the immune system.

The IRS1 mutant models were specifically observed to develop severe resistance in skeletal muscle and liver, with compensatory β-cell hyperplasia. This indicates that resistance is tissue-specific in vivo with IRS1 mutations.

The large docking protein IRS-1 is a major substrate for the receptor and other tyrosine kinases. It plays a key role in eliciting many of 's actions, including binding and activation of phosphatidylinositol (PI) 3-kinase and the subsequent increase in glucose transport.

receptor substrate 1 (IRS-1) is a signaling adapter protein that in humans is encoded by the IRS-1 gene. It is a 131 kDa protein with amino acid sequence of 1242 residues. It contains a single pleckstrin homology (PH) domain at the N-terminus and a PTB domain ca.

IRS1 Gene - Receptor Substrate 1 This gene encodes a protein which is phosphorylated by receptor tyrosine kinase. Mutations in this gene are associated with type II diabetes and susceptibility to resistance.