DSCR1 gene expression is dependent on NFATc1 during cardiac valve formation and colocalizes with anomalous organ development in trisomy 16 mice.

[1]  R. Markwald,et al.  Morphogenetic alterations during endocardial cushion development in the trisomy 16 (Down syndrome) mouse , 2006, Pediatric Cardiology.

[2]  A. Salmi,et al.  Low copy number detection of herpes simplex virus type 1 mRNA and mouse Th1 type cytokine mRNAs by Light Cycler quantitative real-time PCR. , 2003, Journal of virological methods.

[3]  Y. Dor,et al.  VEGF modulates early heart valve formation. , 2003, The anatomical record. Part A, Discoveries in molecular, cellular, and evolutionary biology.

[4]  F. Schoen,et al.  NFATc1 Mediates Vascular Endothelial Growth Factor-induced Proliferation of Human Pulmonary Valve Endothelial Cells* , 2003, The Journal of Biological Chemistry.

[5]  Rick B. Vega,et al.  Dual roles of modulatory calcineurin-interacting protein 1 in cardiac hypertrophy , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[6]  Rick B. Vega,et al.  The role of modulatory calcineurin-interacting proteins in calcineurin signaling. , 2003, Trends in cardiovascular medicine.

[7]  J. Epstein,et al.  Nf1 has an essential role in endothelial cells , 2003, Nature Genetics.

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

[9]  Pascal Kahlem,et al.  A gene expression map of human chromosome 21 orthologues in the mouse , 2002, Nature.

[10]  M. Nemer,et al.  Cooperative interaction between GATA5 and NF-ATc regulates endothelial-endocardial differentiation of cardiogenic cells. , 2002, Development.

[11]  K. Davies,et al.  The DSCR1 (Adapt78) isoform 1 protein calcipressin 1 inhibits calcineurin and protects against acute calcium‐mediated stress damage, including transient oxidative stress , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[12]  William H. Majoros,et al.  A Comparison of Whole-Genome Shotgun-Derived Mouse Chromosome 16 and the Human Genome , 2002, Science.

[13]  G. Crabtree,et al.  NFAT Signaling Choreographing the Social Lives of Cells , 2002, Cell.

[14]  Katherine E Yutzey,et al.  Nkx-2.5 gene induction in mice is mediated by a Smad consensus regulatory region. , 2002, Developmental biology.

[15]  T. Morgan,et al.  Chronic Overexpression of the Calcineurin Inhibitory Gene DSCR1 (Adapt78) Is Associated with Alzheimer's Disease* , 2001, The Journal of Biological Chemistry.

[16]  I. Graef,et al.  NFAT signaling in vertebrate development. , 2001, Current opinion in genetics & development.

[17]  P. Carmeliet,et al.  A novel role for VEGF in endocardial cushion formation and its potential contribution to congenital heart defects. , 2001, Development.

[18]  A. Rao,et al.  Partners in transcription: NFAT and AP-1 , 2001, Oncogene.

[19]  Rick B. Vega,et al.  Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[20]  Eric R. Kandel,et al.  Inducible and Reversible Enhancement of Learning, Memory, and Long-Term Potentiation by Genetic Inhibition of Calcineurin , 2001, Cell.

[21]  X. Estivill,et al.  Dscr1, a novel endogenous inhibitor of calcineurin signaling, is expressed in the primitive ventricle of the heart and during neurogenesis , 2001, Mechanisms of Development.

[22]  J. Slack.  Essential Developmental Biology , 2001 .

[23]  J. Richtsmeier,et al.  Too much of a good thing: mechanisms of gene action in Down syndrome. , 2001, Trends in genetics : TIG.

[24]  E. Olson,et al.  Independent Signals Control Expression of the Calcineurin Inhibitory Proteins MCIP1 and MCIP2 in Striated Muscles , 2000, Circulation research.

[25]  R. P. Thompson,et al.  Conotruncal anomalies in the trisomy 16 mouse: An immunohistochemical analysis with emphasis on the involvement of the neural crest , 2000, The Anatomical record.

[26]  X. Estivill,et al.  DSCR1, overexpressed in Down syndrome, is an inhibitor of calcineurin-mediated signaling pathways. , 2000, Human molecular genetics.

[27]  M. Hattori,et al.  The DNA sequence of human chromosome 21 , 2000, Nature.

[28]  E. Olson,et al.  MEF2 responds to multiple calcium‐regulated signals in the control of skeletal muscle fiber type , 2000, The EMBO journal.

[29]  Rick B. Vega,et al.  A Protein Encoded within the Down Syndrome Critical Region Is Enriched in Striated Muscles and Inhibits Calcineurin Signaling* , 2000, The Journal of Biological Chemistry.

[30]  P. Strippoli,et al.  A new gene family including DSCR1 (Down Syndrome Candidate Region 1) and ZAKI-4: characterization from yeast to human and identification of DSCR1-like 2, a novel human member (DSCR1L2). , 2000, Genomics.

[31]  N. Clipstone,et al.  Identification of Amino Acid Residues and Protein Kinases Involved in the Regulation of NFATc Subcellular Localization* , 2000, The Journal of Biological Chemistry.

[32]  W. Lamers,et al.  Mechanisms of deficient cardiac septation in the mouse with trisomy 16. , 1999, Circulation research.

[33]  H. Toresson,et al.  Retinoids are produced by glia in the lateral ganglionic eminence and regulate striatal neuron differentiation. , 1999, Development.

[34]  K. Yutzey,et al.  Lack of regulation in the heart forming region of avian embryos. , 1999, Developmental biology.

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

[36]  K. Yutzey,et al.  A GATA-dependent nkx-2.5 regulatory element activates early cardiac gene expression in transgenic mice. , 1998, Development.

[37]  J A Epstein,et al.  Neurofibromin modulation of ras activity is required for normal endocardial-mesenchymal transformation in the developing heart. , 1998, Development.

[38]  I. Kola,et al.  Down syndrome and mouse models. , 1998, Current opinion in genetics & development.

[39]  Jeffrey Robbins,et al.  A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.

[40]  Michael J. Grusby,et al.  The transcription factor NF-ATc is essential for cardiac valve formation , 1998, Nature.

[41]  Tak W. Mak,et al.  Role of the NF-ATc transcription factor in morphogenesis of cardiac valves and septum , 1998, Nature.

[42]  H. Winking,et al.  The embryonic development of sensory organs and the skull in the trisomy 16 mouse, an animal model for Down's syndrome. , 1997, Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft.

[43]  T. Hewett,et al.  Cardiac compartment-specific overexpression of a modified retinoic acid receptor produces dilated cardiomyopathy and congestive heart failure in transgenic mice. , 1997, The Journal of clinical investigation.

[44]  X. Estivill,et al.  Genomic organization, alternative splicing, and expression patterns of the DSCR1 (Down syndrome candidate region 1) gene. , 1997, Genomics.

[45]  R. Anderson,et al.  Cardiac morphology at late fetal stages in the mouse with trisomy 16: consequences for different formation of the atrioventricular junction when compared to humans with trisomy 21. , 1997, Cardiovascular research.

[46]  P. Hogan,et al.  Transcription factors of the NFAT family: regulation and function. , 1997, Annual review of immunology.

[47]  G. Crabtree,et al.  Nuclear localization of NF-ATc by a calcineurin-dependent, cyclosporin-sensitive intramolecular interaction. , 1997, Genes & development.

[48]  J. Moreira,et al.  Ocular findings in Down's syndrome. , 1996, American journal of ophthalmology.

[49]  R. Anderson,et al.  Endocardial cushion development and heart loop architecture in the trisomy 16 mouse , 1996, Developmental dynamics : an official publication of the American Association of Anatomists.

[50]  H. Seo,et al.  Molecular Cloning of a Novel Thyroid Hormone-responsive Gene, ZAKI-4, in Human Skin Fibroblasts* , 1996, The Journal of Biological Chemistry.

[51]  Lieve Moons,et al.  Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele , 1996, Nature.

[52]  Kenneth J. Hillan,et al.  Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene , 1996, Nature.

[53]  X. Estivill,et al.  A new human gene from the Down syndrome critical region encodes a proline-rich protein highly expressed in fetal brain and heart. , 1995, Human molecular genetics.

[54]  R. S. Ackley,et al.  Abnormal pinna type and hearing loss correlations in Down's syndrome. , 2008, Journal of intellectual disability research : JIDR.

[55]  C. Disteche,et al.  Down syndrome phenotypes: the consequences of chromosomal imbalance. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[56]  Jane A. Langdale,et al.  In situ Hybridization , 1994 .

[57]  M. Vekemans,et al.  Genetic control of the survival of murine trisomy 16 fetuses. , 1990, Teratology.

[58]  E. Bersu,et al.  Examination of the eyelid closure defect in trisomy 16 mice. , 1990, Teratology.

[59]  J. Rossant,et al.  Inducible expression of an hsp68-lacZ hybrid gene in transgenic mice. , 1989, Development.

[60]  D. Cox,et al.  Mouse Trisomy 16: An Animal Model of Human Trisomy 21 (Down Syndrome) a , 1985, Annals of the New York Academy of Sciences.

[61]  H. Wiśniewski,et al.  Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome , 1985, Annals of neurology.

[62]  H. Winking,et al.  Trisomy 16 in the mouse fetus associated with generalized edema and cardiovascular and urinary tract anomalies. , 1982, Teratology.