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Elizabeth J. Robertson

Researcher at Harvard University

Publications -  75
Citations -  24707

Elizabeth J. Robertson is an academic researcher from Harvard University. The author has contributed to research in topics: Gastrulation & NODAL. The author has an hindex of 54, co-authored 75 publications receiving 23999 citations. Previous affiliations of Elizabeth J. Robertson include Medical Research Council & Vanderbilt University.

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Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r)

TL;DR: In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis.
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Role of Insulin-like Growth Factors in Embryonic and Postnatal Growth

TL;DR: Postnatal growth curves indicated that surviving Igf-1(-/-) mutants, which are infertile and exhibit delayed bone development, continue to grow with a retarded rate after birth in comparison with wild-type littermates and become 30% of normal weight as adults.
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Parental imprinting of the mouse insulin-like growth factor II gene

TL;DR: It is demonstrated that IGF-II is indispensable for normal embryonic growth and that the IGF- II gene is subject to tissue-specific parental imprinting.
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A growth-deficiency phenotype in heterozygous mice carrying an insulin-like growth factor II gene disrupted by targeting.

TL;DR: Germ-line transmission of the inactivated IGF-II gene from male chimaeras yielded heterozygous progeny that were smaller than their ES cell-derived wild-type littermates (about 60% of normal body weight) and these growth-deficient animals were otherwise apparently normal and fertile.
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Erythroid differentiation in chimaeric mice blocked by a targeted mutation in the gene for transcription factor GATA-1

TL;DR: The disruption of the X-linked GATA-1 gene by homologous recombination in a male (XY) murine embryonic stem cell line and testing the Gata-1-deficient cells for their ability to contribute to different tissues in chimaeric mice demonstrates that GATA, the zinc-finger transcription factor, is required for the normal differentiation of erythroid cells, and that other GATAS cannot compensate for its absence.