Abstract
IGF-II plays an important but not pivotal role during normal development in the mouse. By inactivating the endogenous Igf2 gene, DeChiara et al could show that the absence of IGF-II resulted in perfectly healthy and symmetrical offspring although these were 40% smaller than normal littermates (DeChiara et ah 1990). In humans, similar evidence is lacking although genetic data indicate that an overactive IGF2 results in organ hyperplasia as manifested in the Beckwith-Wiedemann syndrome BWS(Junien, 1992). It is interesting in this context that the IGF2 expression patterns during early human development show striking similarities with the organomegaly typical of the BWS (Hedborg et al. 1993).
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Ekström, T.J., Holmgren, L., Glaser, A., Ohlsson, R. (1994). Insulin-Like Growth Factor 2 (IGF2) Expression at the Embryonic/Maternal Boundary. In: Glasser, S.R., Mulholland, J., Psychoyos, A. (eds) Endocrinology of Embryo-Endometrium Interactions. Reproductive Biology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1881-5_20
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