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| Caption | Angiogenesis defects in Tmem100tm1.1Ysai/Tmem100tm1.1Ysai (Tmem100 KO) and Acvrl1tm1Dgen/Acvrl1tm1Dgen (Acvrl1 KO) embryos. (C) Tmem100 null embryos die in utero, showing cardiac dysmorphogenesis and enlargement at E9.5, massive pericardial effusion (arrow) and severe growth retardation at E10.5, and absence of large vitelline vessels in the yolk sac at E10.5. These phenotypes are also observed in Acvrl1 null embryos. (D) Tmem100 null and Acvrl1 null embryos have remarkably similar defects of cardiovascular morphogenesis. Paired dorsal aortas show marked dilatation and narrowing, and clumps of blood cells are frequently seen in the caudal region (asterisk). Mural layers surrounding the aorta and myocardial wall are thinner and ventricular trabeculation is not formed well. The yolk sac shows detachment of endodermal (en) and mesodermal (me) layers and abnormal vessel dilatation. H&E staining at E9.5 is shown. cv, cardinal vein; da, dorsal aorta; isv, intersomitic vessel; nc, notochord; oft, outflow tract; paa, pharyngeal arch artery; ua, umbilical artery; uv, umbilical vein; v, ventricle; va, vitelline artery. (Scale bars: C, 200 um; D, a-i, 50 um; and D, j-l, 20 um.) | ||||||
| Copyright | This image is from Somekawa S, Proc Natl Acad Sci U S A 2012 Jul 24;109(30):12064-9. Copyright 2012 National Academy of Sciences, U.S.A. J:186473 | ||||||
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/19/2024 MGI 6.24 |
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