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.
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5 results for "IGF-I R/IGF1R Proteins and Enzymes" in Products
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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 |
Analyzed by SEC-MALS
Source: | NS0 |
Accession #: | P08069 |
Applications: | Bind |
Source: | CHO |
Accession #: | Q60751 |
Applications: | BA |
Applications: | AC |
Applications: | AC |