Insulin and Insulin-like Receptors
Insulin receptors (IRs) and insulin-like growth factor receptors (IGFRs) are formed from two subunits, each of which is comprised of an extracellular α-subunit and a transmembrane β-subunit with intracellular tyrosine kinase activity. IR homodimers are activated by insulin and, in adults, mediate an increase in glucose uptake through upregulation of GLUT4 expression. Two isoforms of the IR exist: fetal IR-A and adult IR-B.
IGF1R homodimers are activated by IGF-I and IGF-II and mediate pre- and postnatal growth. IGF2R sequesters IGF-II and acts to regulate its levels. IR-IGF1R heterodimers exist and, similar to IGF1R homodimers, are activated by IGF-I and IGF-II. IRs and IGFRs mediate their intracellular actions through the PI3K and RAS/RAF/MAPK signaling pathways and downstream effectors include mTOR, p70 S6 kinase, ERK and JNK.
Many tumors have altered expression of IGF1R and its ligands and this constitutes an early, possible initiating, event in tumorigenesis. Decreases in IR signaling causing 'insulin resistance' is a major component in the development of type 2 diabetes and congenital mutations in the IR can cause the fatal Donohue syndrome.View all products for Insulin and Insulin-like Receptors »
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Literature for Insulin and Insulin-like Receptors
A collection of over 400 products for kinase research, the listing includes inhibitors of:
- Receptor Tyrosine Kinases
- Protein Kinases A, C, D and G
- PI-3 Kinase, Akt and mTOR
- MAPK Signaling
- Receptor Serine/Threonine Kinases
A synopsis of the increasing number of peptides that have been implicated in appetite regulation and energy homeostasis, outlining the putative roles of most of the known proteins and lists compounds available from Tocris.Download PDF | View all reviews
Angiogenesis is the generation of new blood vessels from pre-existing vasculature. It is a hallmark of cancer and plays a key role in enabling tumor growth, progression and metastasis. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster discusses differences between normal angiogenesis physiology, and tumor vascularization, and highlights therapeutic targets aimed at suppressing angiogenesis.Request copy | Download PDF | View all posters