Analysis Tools
mortality/aging
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• homozygous null mice were detected as late as E19.5; embryonic death occurred late in gestation or perinatally
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embryo
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• homozygous null mice displayed a significant size reduction compared with normal and heterozygous littermates
• most embryonic tissues in homozygous null animals appeared grossly normal; however, the intrauterine growth retardation noted in homozygous null embryos suggested that tissues other than the CNS were affected
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• at approximately E8.5, homozygous null embryos exhibited a kinked neural tube
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growth/size/body
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• homozygous null mice displayed a significant size reduction compared with normal and heterozygous littermates
• most embryonic tissues in homozygous null animals appeared grossly normal; however, the intrauterine growth retardation noted in homozygous null embryos suggested that tissues other than the CNS were affected
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nervous system
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• at approximately E8.5, homozygous null embryos exhibited a kinked neural tube
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exencephaly
(
J:63241
)
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• the neural tube defect became more prominent at later stages, and was characterized by a failure of cranial neural tube closure, and eventually by exencephaly
• the neural tubes of homozygous null animals exhibited abnormal Cdkn1b expression, suggesting a neural tube proliferative defect; however, no defects in Cdkn1b regulation or cell cycle control were detected in homozygous null mouse embryo fibroblasts
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