1997
DOI: 10.1073/pnas.94.24.13215
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Abstract: Laron syndrome [growth hormone (GH) insensitivity syndrome] is a hereditary dwarfism resulting from defects in the GH receptor (GHR) gene. GHR deficiency has not been reported in mammals other than humans. Many aspects of GHR dysfunction remain unknown because of ethical and practical limitations in studying humans. To create a mammalian model for this disease, we generated mice bearing a disrupted GHR͞binding protein (GHR͞BP) gene through a homologous gene targeting approach. Homozygous GHR͞BP knockout mice s… Show more

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Cited by 718 publications
(588 citation statements)
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References 50 publications
(52 reference statements)
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“…Growth hormone (GH) resistance or insensitivity with low circulating levels of insulin-like growth factor-1 (IGF1), insulin and glucose, all of which imply increased insulin sensitivity, are among the key characteristics of long-lived GH receptor/binding protein knockout (GHR-KO) mice (1,2). These knockout mice live approximately 40% longer than their normal siblings (3).…”
Section: Introductionmentioning
confidence: 99%
“…Growth hormone (GH) resistance or insensitivity with low circulating levels of insulin-like growth factor-1 (IGF1), insulin and glucose, all of which imply increased insulin sensitivity, are among the key characteristics of long-lived GH receptor/binding protein knockout (GHR-KO) mice (1,2). These knockout mice live approximately 40% longer than their normal siblings (3).…”
Section: Introductionmentioning
confidence: 99%
“…Mice with growth hormone (GH) resistance produced by targeted disruption of the GH receptor/ binding protein gene (GHR/GHBP-KO, hereafter referred to as GHR-KO mice) (Zhou et al 1997) are characterized by normal prenatal growth, major retardation of postnatal growth and adult body size, and a major extension of longevity (Coschigano et al 2003). These animals thrive under a standard feeding regimen, but as adults fail to benefit from a regimen of calorie restriction (CR) that significantly extends longevity of their normal siblings Bonkowski et al 2006).…”
mentioning
confidence: 99%
“…In an effort to better characterize the many roles of GH, and also as a step toward the delineation of IGF-1-dependent and -independent actions, GH signaling was abolished in mice by targeted gene disruption of the GHR/BP gene (Zhou et al 1997). The resulting mouse serves as a mammalian model for the human autosomal recessive disease Laron syndrome, also known as primary GH resistance or insensitivity and as primary IGF-1deficiency (Zhou et al 1997;Kopchick and Laron 1999;Laron et al 1993).…”
mentioning
confidence: 99%
“…The resulting mouse serves as a mammalian model for the human autosomal recessive disease Laron syndrome, also known as primary GH resistance or insensitivity and as primary IGF-1deficiency (Zhou et al 1997;Kopchick and Laron 1999;Laron et al 1993).…”
mentioning
confidence: 99%
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