mortality/aging
• mutant embryos do not survive past E10.5
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cardiovascular system
• starting at E9-E9.5, homozygotes show signs of abnormal formation of cardiac trabeculae
• a significant reduction in cardiac trabeculation is clearly evident by E10.5
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• starting at E9-E9.5, homozygotes display a thinner myocardium; most severe at E10.5
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• at E9.5, mutant hearts fail to show rapid expansion and compaction of the myocardium and do not display the expected increase in volume of the atrium, ventricle and associated structures, indicating a delay in heart development
• however, at E9.5, the extent of apoptosis and cellular proliferation in mutant hearts is comparable to that observed in wild-type hearts
• blood vessel formation appears unaffected and normal fetal and maternal vascular networks are present at E10.5
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• at E9.5 or E10.5, mutant embryos display pericardial edema
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• at E9.5, mutant embryos display a distended pericardial cavity; most severe at E10.5
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hemorrhage
(
J:63049
)
• at E9.5 or E10.5, mutant embryos display hemorrhage in the head and abdominal regions
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muscle
• starting at E9-E9.5, homozygotes show signs of abnormal formation of cardiac trabeculae
• a significant reduction in cardiac trabeculation is clearly evident by E10.5
|
• starting at E9-E9.5, homozygotes display a thinner myocardium; most severe at E10.5
|
homeostasis/metabolism
• at E9.5 or E10.5, mutant embryos display pericardial edema
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embryo
• at E9.5 or E10.5, mutant embryos appear mildly underdeveloped relative to wild-type embryos
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growth/size/body
• at E9.5 or E10.5, mutant embryos appear mildly underdeveloped relative to wild-type embryos
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cellular
• mutant embryonic fibroblasts are highly sensitive to FasL- or TNF-induced apoptosis and exhibit rapid induction of caspase activities
• however, NF-kappaB and JNK/SAPK activation is intact in TNF-stimulated mutant embryonic fibroblasts
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