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IGF-1 displays more binding sites for SHP2 (a phosphatase related to growth) and seems more prone to recruit Cbl [121] (an E3 ligase that targets the receptor for ubiquitination and destruction) and thus may explain a different regulatory mechanism not mediated by serine phosphorylation, and thus not so sensitive to metabolic derangements

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Insulin resistance and increased pancreatic beta-cell proliferation in mice expressing a mutant insulin receptor (P1195L)

Several human studies appear to have been cancelled or stopped without published results a gap that cannot be glossed over clinically [1]