Combined Loss of Hey1 and HeyL Causes Congenital Heart Defects Because of Impaired Epithelial to Mesenchymal Transition
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C. Steidl | P. Jakob | A. Fischer | T. Wagner | E. Lang | P. Friedl | K. Knobeloch | M. Gessler
[1] Raymond B. Runyan,et al. Invasion of mesenchyme into three-dimensional collagen gels: a regional and temporal analysis of interaction in embryonic heart tissue. , 1983, Developmental biology.
[2] D. L. Weeks,et al. Epithelial-mesenchymal transformation of embryonic cardiac endothelial cells is inhibited by a modified antisense oligodeoxynucleotide to transforming growth factor beta 3. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[3] G. Weinmaster,et al. Notch1 is essential for postimplantation development in mice. , 1994, Genes & development.
[4] T. Mak,et al. Disruption of the mouse RBP-J kappa gene results in early embryonic death. , 1995, Development.
[5] R R Markwald,et al. Molecular regulation of atrioventricular valvuloseptal morphogenesis. , 1995, Circulation research.
[6] Paul S. Meltzer,et al. Mutations in the human Jagged1 gene are responsible for Alagille syndrome , 1997, Nature Genetics.
[7] Colin C. Collins,et al. Alagille syndrome is caused by mutations in human Jagged1, which encodes a ligand for Notch1 , 1997, Nature Genetics.
[8] M. Gessler,et al. Developmental expression patterns of mouse sFRP genes encoding members of the secreted frizzled related protein family , 1998, Mechanisms of Development.
[9] S. Artavanis-Tsakonas,et al. Notch signaling: cell fate control and signal integration in development. , 1999, Science.
[10] Manfred Gessler,et al. Hey genes: a novel subfamily of hairy- and Enhancer of split related genes specifically expressed during mouse embryogenesis , 1999, Mechanisms of Development.
[11] H. Macdonald,et al. Deficient T cell fate specification in mice with an induced inactivation of Notch1. , 1999, Immunity.
[12] Wanmin Song,et al. Degradation of type IV collagen by matrix metalloproteinases is an important step in the epithelial-mesenchymal transformation of the endocardial cushions. , 2000, Developmental biology.
[13] M. Gessler,et al. Activation of the Notch pathway in the hair cortex leads to aberrant differentiation of the adjacent hair-shaft layers. , 2000, Development.
[14] D. Srivastava,et al. Members of the HRT family of basic helix-loop-helix proteins act as transcriptional repressors downstream of Notch signaling. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[15] M. Gessler,et al. Comparative analysis of the human and mouse Hey1 promoter: Hey genes are new Notch target genes. , 2000, Biochemical and biophysical research communications.
[16] C. Steidl,et al. Characterization of the human and mouse HEY1, HEY2, and HEYL genes: cloning, mapping, and mutation screening of a new bHLH gene family. , 2000, Genomics.
[17] C. Steidl,et al. Analysis of HeyL expression in wild-type and Notch pathway mutant mouse embryos , 2000, Mechanisms of Development.
[18] A. Hamosh,et al. Familial Tetralogy of Fallot caused by mutation in the jagged1 gene. , 2001, Human molecular genetics.
[19] Y. Bessho,et al. Dynamic expression and essential functions of Hes7 in somite segmentation. , 2001, Genes & development.
[20] L. Kedes,et al. HERP, a Novel Heterodimer Partner of HES/E(spl) in Notch Signaling , 2001, Molecular and Cellular Biology.
[21] J. Hoffman,et al. The incidence of congenital heart disease. , 2002, Journal of the American College of Cardiology.
[22] S. Klewer,et al. Heart-valve mesenchyme formation is dependent on hyaluronan-augmented activation of ErbB2–ErbB3 receptors , 2002, Nature Medicine.
[23] Y. Jan,et al. Tetralogy of Fallot and Other Congenital Heart Defects in Hey2 Mutant Mice , 2002, Current Biology.
[24] R. Bronson,et al. Ventricular septal defect and cardiomyopathy in mice lacking the transcription factor CHF1/Hey2 , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[25] A. Fischer,et al. Mouse gridlock No Aortic Coarctation or Deficiency, but Fatal Cardiac Defects in Hey2 −/− Mice , 2002, Current Biology.
[26] Peter Friedl,et al. Compensation mechanism in tumor cell migration , 2003, The Journal of cell biology.
[27] M. Gessler,et al. Expression of Notch pathway genes in the embryonic mouse metanephros suggests a role in proximal tubule development. , 2003, Gene expression patterns : GEP.
[28] T. Camenisch,et al. Elevated glucose inhibits VEGF-A–mediated endocardial cushion formation , 2003, The Journal of cell biology.
[29] T. Gridley. Notch signaling and inherited disease syndromes. , 2003, Human molecular genetics.
[30] C. Guidos,et al. Notch signaling in development and disease , 2003, Clinical genetics.
[31] S. Neubauer,et al. Rapid identification and 3D reconstruction of complex cardiac malformations in transgenic mouse embryos using fast gradient echo sequence magnetic resonance imaging. , 2003, Journal of molecular and cellular cardiology.
[32] H. Hosokawa,et al. Increased invasion and matrix metalloproteinase-2 expression by Snail-induced mesenchymal transition in squamous cell carcinomas. , 2003, International journal of oncology.
[33] A. Fischer,et al. Hey genes in cardiovascular development. , 2003, Trends in cardiovascular medicine.
[34] Randy L. Johnson,et al. Targeted Disruption of hesr2 Results in Atrioventricular Valve Anomalies That Lead to Heart Dysfunction , 2004, Circulation research.
[35] P. Friedl. Prespecification and plasticity: shifting mechanisms of cell migration. , 2004, Current opinion in cell biology.
[36] A. Fischer,et al. Phenotypic variability in Hey2 −/− mice and absence of HEY2 mutations in patients with congenital heart defects or Alagille syndrome , 2004, Mammalian Genome.
[37] Frank McCormick,et al. Notch promotes epithelial-mesenchymal transition during cardiac development and oncogenic transformation. , 2004, Genes & development.
[38] Linheng Li,et al. Notch Activation Results in Phenotypic and Functional Changes Consistent With Endothelial-to-Mesenchymal Transformation , 2004, Circulation research.
[39] Manfred Gessler,et al. The Notch target genes Hey1 and Hey2 are required for embryonic vascular development. , 2004, Genes & development.
[40] D. Srivastava,et al. Mutations in NOTCH1 cause aortic valve disease , 2005, Nature.
[41] S. Elledge,et al. A lentiviral microRNA-based system for single-copy polymerase II-regulated RNA interference in mammalian cells. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[42] G. Wahl,et al. Reproducible doxycycline-inducible transgene expression at specific loci generated by Cre-recombinase mediated cassette exchange , 2005, Nucleic acids research.
[43] A. Fischer,et al. Hey Basic Helix-Loop-Helix Transcription Factors Are Repressors of GATA4 and GATA6 and Restrict Expression of the GATA Target Gene ANF in Fetal Hearts , 2005, Molecular and Cellular Biology.
[44] Zhiwei Wang,et al. Down-regulation of notch-1 inhibits invasion by inactivation of nuclear factor-kappaB, vascular endothelial growth factor, and matrix metalloproteinase-9 in pancreatic cancer cells. , 2006, Cancer research.