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SOLUTION STRUCTURE OF HUMAN INSULIN-LIKE GROWTH FACTOR II RELATIONSHIP TO RECEPTOR AND BINDING PROTEIN INTERACTIONSSOLUTION STRUCTURE OF HUMAN INSULIN-LIKE GROWTH FACTOR II RELATIONSHIP TO RECEPTOR AND BINDING PROTEIN INTERACTIONS
Structural highlights
DiseaseIGF2_HUMAN Epigenetic changes of DNA hypomethylation in IGF2 are a cause of Silver-Russell syndrome (SRS) [MIM:180860. A clinically heterogeneous condition characterized by severe intrauterine growth retardation, poor postnatal growth, craniofacial features such as a triangular shaped face and a broad forehead, body asymmetry, and a variety of minor malformations. The phenotypic expression changes during childhood and adolescence, with the facial features and asymmetry usually becoming more subtle with age.[1] FunctionIGF2_HUMAN The insulin-like growth factors possess growth-promoting activity. In vitro, they are potent mitogens for cultured cells. IGF-II is influenced by placental lactogen and may play a role in fetal development.[2] Preptin undergoes glucose-mediated co-secretion with insulin, and acts as physiological amplifier of glucose-mediated insulin secretion. Exhibits osteogenic properties by increasing osteoblast mitogenic activity through phosphoactivation of MAPK1 and MAPK3.[3] Evolutionary ConservationCheck, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. See AlsoReferences
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