IGF-I R/IGF1R: Proteins and Enzymes
IGF-I R/IGF1R (Insulin-like Growth Factor I Receptor), also known as CD221, is a ubiquitously expressed heterotetrameric transmembrane glycoprotein consisting of two alpha and two beta subunits. It binds IGF-1 with high affinity, IGF2 with lower affinity, and Insulin with lowest affinity. IGF1R/Insulin R hybrids respond primarily to IGF-1 and may downregulate cellular responses to Insulin. IGF signaling is also modulated by IGF binding proteins and the scavenger receptor, IGF-II R/IGF2R. Mice lacking IGF1R show intrauterine growth deficiency and die at birth due to respiratory failure, and IGF1R mutations in humans can retarded pre- and postnatal growth. IGF-1 and its receptor are particularly important for neurogenesis, with deficiency producing microcephaly and learning disorders. IGF1R expression on human embryonic stem cells is important for their survival and clonogenicity.
Products:
6 results for "IGF-I R/IGF1R Proteins and Enzymes" in Products
6 results for "IGF-I R/IGF1R Proteins and Enzymes" in Products
IGF-I R/IGF1R: Proteins and Enzymes
IGF-I R/IGF1R (Insulin-like Growth Factor I Receptor), also known as CD221, is a ubiquitously expressed heterotetrameric transmembrane glycoprotein consisting of two alpha and two beta subunits. It binds IGF-1 with high affinity, IGF2 with lower affinity, and Insulin with lowest affinity. IGF1R/Insulin R hybrids respond primarily to IGF-1 and may downregulate cellular responses to Insulin. IGF signaling is also modulated by IGF binding proteins and the scavenger receptor, IGF-II R/IGF2R. Mice lacking IGF1R show intrauterine growth deficiency and die at birth due to respiratory failure, and IGF1R mutations in humans can retarded pre- and postnatal growth. IGF-1 and its receptor are particularly important for neurogenesis, with deficiency producing microcephaly and learning disorders. IGF1R expression on human embryonic stem cells is important for their survival and clonogenicity.
Products:
| Source: | NS0 |
| Accession #: | P08069 |
| Applications: | Bind |
| Source: | NS0 |
| Accession #: | P08069 |
| Applications: | Bind |
| Source: | CHO |
| Accession #: | Q60751 |
| Applications: | BA |
| Source: | HEK293 |
| Applications: | BA |
