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http://purl.uniprot.org/citations/8402901http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/8402901http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/8402901http://www.w3.org/2000/01/rdf-schema#comment"Newborn mice homozygous for a targeted disruption of insulin-like growth factor gene (Igf-1) exhibit a growth deficiency similar in severity to that previously observed in viable Igf-2 null mutants (60% of normal birthweight). Depending on genetic background, some of the Igf-1(-/-) dwarfs die shortly after birth, while others survive and reach adulthood. In contrast, null mutants for the Igf1r gene die invariably at birth of respiratory failure and exhibit a more severe growth deficiency (45% normal size). 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. Igf-1(-/-)/Igf1r(-/-) double mutants did not differ in phenotype from Igf1r(-/-) single mutants, while in Igf-2(-)/Igf1r(-/-) and Igf-1(-/-)/Igf-2(-) double mutants, which are phenotypically identical, the dwarfism was further exacerbated (30% normal size). The roles of the IGFs in mouse embryonic development, as revealed from the phenotypic differences between these mutants, are discussed."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.org/dc/terms/identifier"doi:10.1016/s0092-8674(05)80084-4"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.org/dc/terms/identifier"doi:10.1016/s0092-8674(05)80084-4"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Baker J."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Baker J."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Robertson E.J."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Robertson E.J."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Efstratiadis A."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Efstratiadis A."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Liu J.P."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Liu J.P."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Perkins A.S."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/author"Perkins A.S."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/date"1993"xsd:gYear
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/date"1993"xsd:gYear
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/name"Cell"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/name"Cell"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/pages"59-72"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/pages"59-72"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/title"Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r)."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/title"Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r)."xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/volume"75"xsd:string
http://purl.uniprot.org/citations/8402901http://purl.uniprot.org/core/volume"75"xsd:string