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- W2064308078 endingPage "206" @default.
- W2064308078 startingPage "185" @default.
- W2064308078 abstract "The type 1 Simpson-Golabi-Behmel overgrowth syndrome (SGBS1) is caused by loss-of-function mutations of the X-linked GPC3 gene encoding glypican-3, a cell-surface heparan sulfate proteoglycan that apparently plays a negative role in growth control by an unknown mechanism. Mice carrying a Gpc3 gene knockout exhibited several phenotypic features that resemble clinical hallmarks of SGBS1, including somatic overgrowth, renal dysplasia, accessory spleens, polydactyly, and placentomegaly. In Gpc3/DeltaH19 double mutants (lacking GPC3 and also carrying a deletion around the H19 gene region that causes bialellic expression of the closely linked Igf2 gene by imprint relaxation), the Gpc3-null phenotype was exacerbated, while additional SGBS1 features (omphalocele and skeletal defects) were manifested. However, results from a detailed comparative analysis of growth patterns in double mutants lacking GPC3 and also IGF2, IGF1, or the type 1 IGF receptor (IGF1R) provided conclusive genetic evidence inconsistent with the hypothesis that GPC3 acts as a growth suppressor by sequestering or downregulating an IGF ligand. Nevertheless, our data are compatible with a model positing that there is downstream convergence of the independent signaling pathways in which either IGFs or (indirectly) GPC3 participate." @default.
- W2064308078 created "2016-06-24" @default.
- W2064308078 creator A5003632912 @default.
- W2064308078 creator A5031552464 @default.
- W2064308078 creator A5036271984 @default.
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- W2064308078 creator A5076894699 @default.
- W2064308078 creator A5079340049 @default.
- W2064308078 creator A5085568887 @default.
- W2064308078 date "2002-03-01" @default.
- W2064308078 modified "2023-10-18" @default.
- W2064308078 title "Overgrowth of a Mouse Model of the Simpson–Golabi–Behmel Syndrome Is Independent of IGF Signaling" @default.
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