Norrin, Frizzled-4, and Lrp5 Signaling in Endothelial Cells Controls a Genetic Program for Retinal Vascularization

[1]  Calvin J Kuo,et al.  Wnt/β-catenin signaling is required for CNS, but not non-CNS, angiogenesis , 2009, Proceedings of the National Academy of Sciences.

[2]  A. McMahon,et al.  Canonical Wnt Signaling Regulates Organ-Specific Assembly and Differentiation of CNS Vasculature , 2008, Science.

[3]  M. McCall,et al.  Comparisons of structural and functional abnormalities in mouse b‐wave mutants , 2008, The Journal of physiology.

[4]  M. Wang,et al.  A model for familial exudative vitreoretinopathy caused by LPR5 mutations. , 2008, Human molecular genetics.

[5]  J. Martial,et al.  Zebrafish Sox7 and Sox18 function together to control arterial-venous identity. , 2008, Developmental biology.

[6]  S. Feil,et al.  Vascular changes in the cerebellum of Norrin /Ndph knockout mice correlate with high expression of Norrin and Frizzled‐4 , 2008, The European journal of neuroscience.

[7]  Jeremy Nathans,et al.  The Optokinetic Reflex as a Tool for Quantitative Analyses of Nervous System Function in Mice: Application to Genetic and Drug-Induced Variation , 2008, PloS one.

[8]  Y. Saijoh,et al.  Redundant roles of Sox17 and Sox18 in early cardiovascular development of mouse embryos. , 2007, Biochemical and biophysical research communications.

[9]  K. Alitalo,et al.  Molecular regulation of angiogenesis and lymphangiogenesis , 2007, Nature Reviews Molecular Cell Biology.

[10]  R. Schwartz,et al.  Sox17 is essential for the specification of cardiac mesoderm in embryonic stem cells , 2007, Proceedings of the National Academy of Sciences.

[11]  T. Tahira,et al.  Severe Form of Familial Exudative Vitreoretinopathy Caused by Homozygous R417Q Mutation in Frizzled-4 Gene , 2007, Ophthalmic genetics.

[12]  J. Nathans,et al.  Mutational Analysis of Norrin-Frizzled4 Recognition* , 2006, Journal of Biological Chemistry.

[13]  R. Hiramatsu,et al.  Redundant roles of Sox17 and Sox18 in postnatal angiogenesis in mice , 2006, Journal of Cell Science.

[14]  J. Wittbrodt,et al.  Rx‐Cre, a tool for inactivation of gene expression in the developing retina , 2006, Genesis.

[15]  R. Adams,et al.  Ephrin-B2 Controls Cell Motility and Adhesion during Blood-Vessel-Wall Assembly , 2006, Cell.

[16]  T. Gardner,et al.  Retinal angiogenesis in development and disease , 2005, Nature.

[17]  W. Berger,et al.  Mice Null for Frizzled4 (Fzd4−/−) Are Infertile and Exhibit Impaired Corpora Lutea Formation and Function1 , 2005, Biology of reproduction.

[18]  Minrong Ai,et al.  Clinical and molecular findings in osteoporosis-pseudoglioma syndrome. , 2005, American journal of human genetics.

[19]  C. Betsholtz,et al.  Endothelial/Pericyte Interactions , 2005, Circulation research.

[20]  C. Grimm,et al.  Role of the Norrie disease pseudoglioma gene in sprouting angiogenesis during development of the retinal vasculature. , 2005, Investigative ophthalmology & visual science.

[21]  W. Berger,et al.  Fetal loss in homozygous mutant Norrie disease mice: A new role of Norrin in reproduction , 2005, Genesis.

[22]  T. Tahira,et al.  Complexity of the genotype–phenotype correlation in familial exudative vitreoretinopathy with mutations in the LRP5 and/or FZD4 genes , 2005, Human mutation.

[23]  M. Reed,et al.  Matricellular homologs in the foreign body response: hevin suppresses inflammation, but hevin and SPARC together diminish angiogenesis. , 2005, The American journal of pathology.

[24]  M. Seeliger,et al.  Ectopic Norrin Induces Growth of Ocular Capillaries and Restores Normal Retinal Angiogenesis in Norrie Disease Mutant Mice , 2005, The Journal of Neuroscience.

[25]  M. Trese,et al.  Autosomal recessive familial exudative vitreoretinopathy is associated with mutations in LRP5. , 2004, American journal of human genetics.

[26]  H. Firth,et al.  Norrie disease and peripheral venous insufficiency , 2004, British Journal of Ophthalmology.

[27]  E. Lütjen-Drecoll,et al.  Norrie gene product is necessary for regression of hyaloid vessels. , 2004, Investigative ophthalmology & visual science.

[28]  Michael J Parker,et al.  Mutations in LRP5 or FZD4 underlie the common familial exudative vitreoretinopathy locus on chromosome 11q. , 2004, American journal of human genetics.

[29]  J. Nathans,et al.  Vascular Development in the Retina and Inner Ear Control by Norrin and Frizzled-4, a High-Affinity Ligand-Receptor Pair , 2004, Cell.

[30]  M. Biel,et al.  Melanopsin and rod–cone photoreceptive systems account for all major accessory visual functions in mice , 2003, Nature.

[31]  Xiaojing Su,et al.  Isolation and characterization of murine retinal endothelial cells. , 2003, Molecular vision.

[32]  A. McMahon,et al.  Efficient gene modulation in mouse epiblast using a Sox2Cre transgenic mouse strain , 2002, Mechanisms of Development.

[33]  A. McMahon,et al.  Efficient gene modulation in mouse epiblast using a Sox2Cre transgenic mouse strain. , 2002, Gene expression patterns : GEP.

[34]  S. Wu,et al.  Adler's Physiology of the Eye , 2002 .

[35]  M. Hayden,et al.  Mutant frizzled-4 disrupts retinal angiogenesis in familial exudative vitreoretinopathy , 2002, Nature Genetics.

[36]  H. Rehm,et al.  Vascular Defects and Sensorineural Deafness in a Mouse Model of Norrie Disease , 2002, The Journal of Neuroscience.

[37]  C. Hartmann,et al.  Cbfa1-independent decrease in osteoblast proliferation, osteopenia, and persistent embryonic eye vascularization in mice deficient in Lrp5, a Wnt coreceptor , 2002, The Journal of cell biology.

[38]  J. Nathans,et al.  Progressive Cerebellar, Auditory, and Esophageal Dysfunction Caused by Targeted Disruption of thefrizzled-4 Gene , 2001, The Journal of Neuroscience.

[39]  R. Hammer,et al.  Tie2-Cre transgenic mice: a new model for endothelial cell-lineage analysis in vivo. , 2001, Developmental biology.

[40]  C. Scriver.  The Metabolic and Molecular Bases of Inherited Disease , 2001 .

[41]  E. Barrón,et al.  Isolation and culture of rat retinal microvessel endothelial cells using magnetic beads coated with antibodies to PECAM-1 , 2000, Current eye research.

[42]  C. Lobe,et al.  Z/AP, a double reporter for cre-mediated recombination. , 1999, Developmental biology.

[43]  W. Berger,et al.  Retinal vasculature changes in Norrie disease mice. , 1998, Investigative ophthalmology & visual science.

[44]  M. Trese,et al.  Identification of missense mutations in the Norrie disease gene associated with advanced retinopathy of prematurity. , 1997, Archives of ophthalmology.

[45]  S. Nakanishi,et al.  Impairment of Pupillary Responses and Optokinetic Nystagmus in the mGluR6-deficient Mouse , 1997, Neuropharmacology.

[46]  T. Springer,et al.  Modulation of Endothelial Cell Adhesion by Hevin, an Acidic Protein Associated with High Endothelial Venules (*) , 1996, The Journal of Biological Chemistry.

[47]  Y. Fujiwara,et al.  Vascular endothelial cell lineage-specific promoter in transgenic mice. , 1995, Development.

[48]  Markus Meister,et al.  Multi-neuronal signals from the retina: acquisition and analysis , 1994, Journal of Neuroscience Methods.

[49]  D. Kioussis,et al.  Direct derivation of conditionally immortal cell lines from an H-2Kb-tsA58 transgenic mouse. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[50]  Angus M'Gillivray,et al.  The Ocular Circulation , 1904, Edinburgh Medical Journal.

[51]  B. Wilcken.  THE METABOLIC AND MOLECULAR BASES OF INHERITED DISEASE , 2010 .

[52]  Charles E. Riva,et al.  Ocular circulation in Adler's Physiology of the Eye. : Nutrition of the eye. , 2003 .

[53]  N. Okamoto.  [Norrie disease]. , 1998, Ryoikibetsu shokogun shirizu.

[54]  H. Rehm,et al.  Norrie disease gene mutation in a large Costa Rican kindred with a novel phenotype including venous insufficiency , 1997, Human mutation.

[55]  D. Kioussis,et al.  H‐2Kb‐tsA58トランスジェニックマウスから直接に無限増殖細胞系を得る方法 , 1991 .