Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects

• Main Authors: Bard-Chapeau E.A., Szumska D., Jacob B., Chua B.Q.L., Chatterjee G.C., Zhang Y., Ward J.M., Urun F., Kinameri E., Vincent S.D., Ahmed S., Bhattacharya S., Osato M., Perkins A.S., Moore A.W., Jenkins N.A., Copeland N.G.
• Other Authors: CANCER SCIENCE INSTITUTE OF SINGAPORE
• Format: Article
• Published: 2019
• Subjects: adult; allele; amino terminal sequence; animal cell; animal experiment; animal model; animal tissue; article; binding site; congenital heart malformation; controlled study; disease severity; embryo; embryo development; EVI1 gene; exon; gene deletion; gene function; gene identification; gene location; gene silencing; gene targeting; germ line; hematopoietic cell; heterozygote; lethality; mouse; newborn; nonhuman; perinatal period; phenotype; regulator gene; transcription initiation site; Alleles; Animals; Animals, Newborn; Base Sequence; Bone Marrow; Disease Models, Animal; DNA-Binding Proteins; Exons; Gene Deletion; Gene Expression Regulation, Developmental; Genes, Lethal; Genetic Association Studies; Heart Defects, Congenital; Hematopoiesis; Hematopoietic Stem Cells; Immunophenotyping; Mice; Mice, Knockout; Molecular Sequence Data; Mutation; Phenotype; Proto-Oncogenes; Sequence Alignment; Severity of Illness Index; Transcription Factors
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/161427
• Institution: National University of Singapore

10.1371/journal.pone.0089397