The pattern of congenital heart defects arising from reduced Tbx5 expression is altered in a Down syndrome mouse model

[1]  Derek E Anane BMC Developmental Biology reviewer acknowledgement 2015 , 2016, BMC Developmental Biology.

[2]  Jacqueline H. Finger,et al.  GXD: a community resource of mouse Gene Expression Data , 2015, Mammalian Genome.

[3]  J. Richtsmeier,et al.  Overlapping trisomies for human chromosome 21 orthologs produce similar effects on skull and brain morphology of Dp(16)1Yey and Ts65Dn mice , 2014, American journal of medical genetics. Part A.

[4]  S. Conway,et al.  Cardiac outflow tract anomalies , 2013, Wiley interdisciplinary reviews. Developmental biology.

[5]  Lora J. H. Bean,et al.  An excess of deleterious variants in VEGF-A pathway genes in Down-syndrome-associated atrioventricular septal defects. , 2012, American journal of human genetics.

[6]  C. Maslen,et al.  Genetic Modifiers Predisposing to Congenital Heart Disease in the Sensitized Down Syndrome Population , 2012, Circulation. Cardiovascular genetics.

[7]  S. Bhattacharya,et al.  Pitx2 confers left morphological, molecular, and functional identity to the sinus venosus myocardium , 2011, Cardiovascular research.

[8]  Yueming Ding,et al.  Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn , 2011, Mammalian Genome.

[9]  Y. Hérault,et al.  Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling down syndrome , 2011, Mammalian Genome.

[10]  Aibin He,et al.  Co-occupancy by multiple cardiac transcription factors identifies transcriptional enhancers active in heart , 2011, Proceedings of the National Academy of Sciences.

[11]  Mary Goldman,et al.  The UCSC Genome Browser database: update 2011 , 2010, Nucleic Acids Res..

[12]  Michael K Gross,et al.  Pitx2-dependent Occupancy by Histone Deacetylases Is Associated with T-box Gene Regulation in Mammalian Abdominal Tissue*♦ , 2010, The Journal of Biological Chemistry.

[13]  Scott F. Gilbert,et al.  Reptilian heart development and the molecular basis of cardiac chamber evolution , 2009, Nature.

[14]  J. Friedland-Little,et al.  sonic hedgehog is required in pulmonary endoderm for atrial septation , 2009, Development.

[15]  Ting Wang,et al.  The UCSC Genome Browser Database: update 2009 , 2008, Nucleic Acids Res..

[16]  Austin D. Williams,et al.  Characterization of the cardiac phenotype in neonatal Ts65Dn mice , 2008, Developmental dynamics : an official publication of the American Association of Anatomists.

[17]  K. Furie,et al.  Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. , 2008, Circulation.

[18]  R. Roper,et al.  The power of comparative and developmental studies for mouse models of Down syndrome , 2007, Mammalian Genome.

[19]  C. S. Moore Postnatal lethality and cardiac anomalies in the Ts65Dn Down Syndrome mouse model , 2006, Mammalian Genome.

[20]  Kazuko Koshiba-Takeuchi,et al.  Tbx5-dependent rheostatic control of cardiac gene expression and morphogenesis. , 2006, Developmental biology.

[21]  B. Black,et al.  Pitx2 regulates cardiac left-right asymmetry by patterning second cardiac lineage-derived myocardium. , 2006, Developmental biology.

[22]  M. Iruela-Arispe,et al.  Proteolytic cleavage of versican during cardiac cushion morphogenesis , 2006, Developmental dynamics : an official publication of the American Association of Anatomists.

[23]  H. Hamada,et al.  Conserved regulation and role of Pitx2 in situs-specific morphogenesis of visceral organs , 2006, Development.

[24]  B. Morrow,et al.  Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field , 2006, Development.

[25]  R. Reeves,et al.  Perinatal Loss of Ts65Dn Down Syndrome Mice , 2006, Genetics.

[26]  C. Stoll,et al.  Epidemiology of Down syndrome in 118,265 consecutive births. , 2005, American journal of medical genetics. Supplement.

[27]  J. Borlak,et al.  TBX5 mutations in Non‐Holt‐Oram Syndrome (HOS) malformed hearts , 2004, Human mutation.

[28]  M. Iruela-Arispe,et al.  ADAMTS1/METH1 Inhibits Endothelial Cell Proliferation by Direct Binding and Sequestration of VEGF165* , 2003, Journal of Biological Chemistry.

[29]  D. Franco,et al.  The role of Pitx2 during cardiac development. Linking left-right signaling and congenital heart diseases. , 2003, Trends in cardiovascular medicine.

[30]  J. Schug Using TESS to Predict Transcription Factor Binding Sites in DNA Sequence , 2003, Current protocols in bioinformatics.

[31]  Gregor Eichele,et al.  Human chromosome 21 gene expression atlas in the mouse , 2002, Nature.

[32]  Donna M. Martin,et al.  Pitx2 distinguishes subtypes of terminally differentiated neurons in the developing mouse neuroepithelium. , 2002, Developmental biology.

[33]  Thomas D. Schmittgen,et al.  Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.

[34]  J. Schmitt,et al.  A Murine Model of Holt-Oram Syndrome Defines Roles of the T-Box Transcription Factor Tbx5 in Cardiogenesis and Disease , 2001, Cell.

[35]  E. A. Packham,et al.  Characterization of the TBX5 binding site and analysis of mutations that cause Holt-Oram syndrome. , 2001, Human molecular genetics.

[36]  A. McMahon,et al.  Smoothened Mutants Reveal Redundant Roles for Shh and Ihh Signaling Including Regulation of L/R Asymmetry by the Mouse Node , 2001, Cell.

[37]  J. Martín,et al.  Regulation of left-right asymmetry by thresholds of Pitx2c activity. , 2001, Development.

[38]  A. Moorman,et al.  Pitx2 expression defines a left cardiac lineage of cells: evidence for atrial and ventricular molecular isomerism in the iv/iv mice. , 2001, Developmental biology.

[39]  G. Mortier,et al.  Hemiplegic cerebral palsy and the factor V Leiden mutation , 2000, Journal of medical genetics.

[40]  S. Miyagawa-Tomita,et al.  Mouse Pitx2 deficiency leads to anomalies of the ventral body wall, heart, extra- and periocular mesoderm and right pulmonary isomerism. , 1999, Development.

[41]  S. Camper,et al.  Dosage requirement of Pitx2 for development of multiple organs. , 1999, Development.

[42]  Concepción Rodríguez-Esteban,et al.  Multiple left-right asymmetry defects in Shh(-/-) mutant mice unveil a convergence of the shh and retinoic acid pathways in the control of Lefty-1. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[43]  M. Rosenfeld,et al.  Pitx2 regulates lung asymmetry, cardiac positioning and pituitary and tooth morphogenesis , 1999, Nature.

[44]  Randy L. Johnson,et al.  Function of Rieger syndrome gene in left–right asymmetry and craniofacial development , 1999, Nature.

[45]  J. Seidman,et al.  Chamber-specific cardiac expression of Tbx5 and heart defects in Holt-Oram syndrome. , 1999, Developmental biology.

[46]  M. Khoury,et al.  Population-based study of congenital heart defects in Down syndrome. , 1998, American journal of medical genetics.

[47]  C. Tabin,et al.  The Transcription Factor Pitx2 Mediates Situs-Specific Morphogenesis in Response to Left-Right Asymmetric Signals , 1998, Cell.

[48]  J. C. Belmonte,et al.  Pitx2 determines left–right asymmetry of internal organs in vertebrates , 1998, Nature.

[49]  R. Newbury-Ecob,et al.  Holt-Oram syndrome: a clinical genetic study. , 1996, Journal of medical genetics.

[50]  R. Bronson,et al.  A mouse model for Down syndrome exhibits learning and behaviour deficits , 1995, Nature Genetics.

[51]  E. Colvin,et al.  Congenital Heart Disease in Infants With Down's Syndrome , 1994, Southern medical journal.

[52]  M. Khoury,et al.  Improved ascertainment of cardiovascular malformations in infants with Down's syndrome, Atlanta, 1968 through 1989. Implications for the interpretation of increasing rates of cardiovascular malformations in surveillance systems. , 1992, American journal of epidemiology.

[53]  P. Pradat Epidemiology of major congenital heart defects in Sweden, 1981-1986. , 1992, Journal of epidemiology and community health.

[54]  Lorna Richardson,et al.  EMAGE: Electronic Mouse Atlas of Gene Expression. , 2014, Methods in molecular biology.

[55]  R. Reeves,et al.  A Sonic hedgehog (Shh) response deficit in trisomic cells may be a common denominator for multiple features of Down syndrome. , 2012, Progress in brain research.

[56]  J. Seidman,et al.  Mutations in human TBX5 [corrected] cause limb and cardiac malformation in Holt-Oram syndrome. , 1997, Nature genetics.

[57]  David I. Wilson,et al.  Holt-Oram syndrome is caused by mutations in TBX5, a member of the Brachyury (T) gene family , 1997, Nature Genetics.

[58]  R. Kucherlapati,et al.  Mutations in human cause limb and cardiac malformation in Holt-Oram syndrome , 1997, Nature Genetics.

[59]  J. Seidman,et al.  Erratum: Mutations in human TBX5 cause limb and cardiac malformation in Holt-Oram syndrome , 1997, Nature Genetics.

[60]  L. W. Perry,et al.  Congenital cardiovascular malformations associated with chromosome abnormalities: an epidemiologic study. , 1989, The Journal of pediatrics.