Abstract
DLC-1 (deleted in liver cancer 1) is a Rho GTPase-activating protein that is able to inhibit cell growth and suppress tumorigenesis. We have used homologous recombination to inactivate the mouse DLC-1 gene (Arhgap7). Mice heterozygous for the targeted allele were phenotypically normal, but homozygous mutant embryos did not survive beyond 10.5 days post coitum. Histological analysis revealed that DLC-1-/- embryos had defects in the neural tube, brain, heart, and placenta. Cultured fibroblasts from DLC-1-deficient embryos displayed alterations in the organization of actin filaments and focal adhesions.
MeSH terms
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Animals
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Cells, Cultured
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Cytoskeleton / genetics
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Cytoskeleton / metabolism
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Cytoskeleton / pathology
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Embryo, Mammalian / embryology*
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Embryo, Mammalian / metabolism*
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Fibroblasts
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GTPase-Activating Proteins / deficiency
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GTPase-Activating Proteins / genetics
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GTPase-Activating Proteins / metabolism*
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Gene Deletion
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Gene Expression Regulation, Developmental
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Heterozygote
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Mice
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Mice, Knockout
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Mutation / genetics
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Transcription, Genetic / genetics
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Tumor Suppressor Proteins / deficiency
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism*
Substances
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DLC-1 (deleted in liver cancer) protein, mouse
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GTPase-Activating Proteins
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RNA, Messenger
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Tumor Suppressor Proteins