Florentia M. Smith

TL;DR: The results indicate that changes in GRB10 dosage could, in at least some cases, account for the severe growth retardation that is characteristic of Silver–Russell syndrome and provides evidence that imprinting acts on at least two major fetal growth axes in a manner consistent with parent–offspring conflict theory.

TL;DR: It is demonstrated that within the brain Grb10 is expressed from the paternal allele from fetal life into adulthood and that ablation of this expression engenders increased social dominance specifically among other aspects of social behaviour, a finding supported by the observed increase in allogrooming by paternal Grb 10-deficient animals.

TL;DR: A small sub-set of mammalian genes are subject to regulation by genomic imprinting such that only one parental allele is active in at least some sites of expression, and a number of imprinted genes have been found to influence energy homeostasis and some, including Igf2 and Grb10, may coordinate growth with glucose-regulated metabolism.

TL;DR: Tissue-specific changes in insulin receptor tyrosine phosphorylation were consistent with a model in which Grb10, like the closely related Grb14 adapter protein, prevents specific protein tyrosin phosphatases from accessing phosphorylated tyrosines within the kinase activation loop.

TL;DR: It is shown that following disruption of the maternal allele in mice, the labyrinthine volume was increased in a manner consistent with a cell-autonomous function of Grb10 and the enlarged placenta was more efficient in supporting foetal growth, becoming the first example of a gene that acts to limit placental size and efficiency.