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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)

Mice Carrying Null Mutations of the Genes Encoding Insulin-Like Growth Factor I (Igf-1) and Type 1 IGF Receptor (Igf1r)

J P Liu, J Baker, A S Perkins, E J Robertson, A Efstratiadis

Cell. 1993 Oct 8;75(1):59-72.

PMID: 8402901

Abstract:

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248143	Insulin-like Growth Factor-I from mouse			Price

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