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Journal Article
Journal of Bone and Mineral Research, ISSN 0884-0431, 08/2012, Volume 27, Issue 8, pp. 1757 - 1772
Chronic kidney disease–mineral bone disorder (CKD‐MBD) is defined by abnormalities in mineral and hormone metabolism, bone histomorphometric changes, and/or... 
RENAL OSTEODYSTROPHY | OSTEOCYTE | WNT/β‐CATENIN | WNT/β-CATENIN | AORTIC CALCIFICATION | VASCULAR CALCIFICATION | ss-CATENIN | MINERAL BONE DISORDER | BETA-CATENIN | NONDIALYZED PATIENTS | CORONARY-ARTERY CALCIFICATION | ENDOCRINOLOGY & METABOLISM | CARDIOVASCULAR-DISEASE | HEMODIALYSIS-PATIENTS | PARATHYROID-HORMONE | WNT | CHRONIC KIDNEY-DISEASE | Bone and Bones - pathology | Chronic Kidney Disease-Mineral and Bone Disorder - pathology | Chronic Kidney Disease-Mineral and Bone Disorder - blood | Humans | Middle Aged | Chronic Kidney Disease-Mineral and Bone Disorder - physiopathology | Glycoproteins - metabolism | Cardiovascular Abnormalities - blood | Male | Chronic Kidney Disease-Mineral and Bone Disorder - metabolism | Gene Expression Profiling | Cardiovascular Abnormalities - pathology | Cardiovascular Abnormalities - physiopathology | Kidney Failure, Chronic - pathology | Bone and Bones - metabolism | Female | Kidney Failure, Chronic - physiopathology | Osteoclasts - pathology | Cardiovascular Abnormalities - complications | Osteocytes - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Mutation - genetics | Osteoclasts - metabolism | Disease Progression | Animals | Kidney Failure, Chronic - blood | Wnt Signaling Pathway - genetics | Biopsy | Calcification, Physiologic | Kidney Failure, Chronic - complications | Osteocytes - pathology | Mice | Bone Remodeling | NIMA-Related Kinases | Vascular Calcification | Calcification (ectopic) | Renal function | Renal osteodystrophy | Wnt protein | Polycystic kidney | catenin | Osteocytes | Bone diseases | Minerals | Gene expression | Osteoprotegerin | Gene silencing | Signal transduction | NF- Kappa B protein | Osteoclasts | Kidney diseases | TRANCE protein | Age | Osteogenesis
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2013, Volume 110, Issue 21, pp. 8621 - 8626
Journal Article
Journal Article
Journal Article
Developmental Biology, ISSN 0012-1606, 11/2013, Volume 383, Issue 2, pp. 239 - 252
Neural crest cells (NCCs) are physically responsible for craniofacial skeleton formation, pharyngeal arch artery remodeling and cardiac outflow tract septation... 
Neural crest cell | Persistent truncus arteriosus | GTPase | Migration | Cdc42 | Craniofacial malformation | CARDIAC OUTFLOW TRACT | HEART FIELD | MOUSE EMBRYOS | G-PROTEINS | DEVELOPMENTAL BIOLOGY | NUCLEOTIDE EXCHANGE FACTOR | MICE | FOCAL ADHESION KINASE | ACTIN CYTOSKELETON | RHO-GTPASES | Bone Morphogenetic Protein 2 - pharmacology | Embryo, Mammalian - drug effects | Neural Crest - pathology | Actins - metabolism | Craniofacial Abnormalities - embryology | Male | cdc42 GTP-Binding Protein - metabolism | Pseudopodia - drug effects | Cardiovascular Abnormalities - pathology | Gene Deletion | Thymus Gland - pathology | Craniofacial Abnormalities - pathology | Female | Neural Crest - enzymology | Embryo, Mammalian - pathology | Osteogenesis - drug effects | Genotype | Cardiovascular Abnormalities - embryology | Thymus Gland - drug effects | Enzyme Activation - drug effects | Embryo, Mammalian - abnormalities | Mice, Knockout | Neural Crest - drug effects | Cardiovascular Abnormalities - enzymology | Cell Movement - drug effects | Thymus Gland - abnormalities | Phenotype | Animals | Pseudopodia - metabolism | Cell Differentiation - drug effects | Craniofacial Abnormalities - enzymology | Cytoskeleton - metabolism | Morphogenesis - drug effects | Mice | Crosses, Genetic | Embryonic development | Lubrication and lubricants | Analysis | Medical genetics | Bone morphogenetic proteins | Neovascularization | Binding proteins | Protein binding
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 12/2010, Volume 30, Issue 12, pp. 2575 - 2586
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2012, Volume 109, Issue 6, pp. 2015 - 2020
Normal vision requires the precise control of vascular growth to maintain corneal transparency. Here we provide evidence for a unique mechanism by which the... 
Angiogenesis | Cornea | Blood vessels | Mice | Physical trauma | Lymphatic vessels | Corneal neovascularization | Genetic mutation | Embryos | Endothelial cells | Soluble form of VEGF receptor 1 | VEGF bioavailablility | Avascularity | DNA METHYLATION | MULTIDISCIPLINARY SCIENCES | KEY PLAYERS | CARDIOVASCULAR DEVELOPMENT | MATRIX METALLOPROTEINASES | AXENFELD-RIEGER-SYNDROME | RETINOIC ACID | ENDOTHELIAL-CELLS | soluble form of VEGF receptor 1 | avascularity | EXTRACELLULAR-MATRIX | NEURAL CREST | HELIX GENE | Blood Vessels - growth & development | Blood Vessels - pathology | Neural Crest - pathology | Vascular Endothelial Growth Factor A - metabolism | Anterior Eye Segment - abnormalities | Neovascularization, Pathologic - pathology | Neural Crest - metabolism | Anterior Eye Segment - metabolism | Pupil | Cornea - blood supply | Forkhead Transcription Factors - metabolism | Cornea - pathology | Corneal Stroma - enzymology | Lymphangiogenesis | Eye Abnormalities - metabolism | Alkalies | Haploinsufficiency - genetics | Signal Transduction | Anterior Eye Segment - pathology | Mutation - genetics | Phenotype | Animals | Eye Abnormalities - pathology | Burns - pathology | Corneal Stroma - pathology | Heterozygote | Neovascularization, Pathologic - metabolism | Matrix Metalloproteinases - metabolism | Eye Abnormalities - complications | Transcription factors | Physiological aspects | Genetic aspects | Neovascularization | Research | Vascular endothelial growth factor | Biological Sciences
Journal Article