Indexed keywords
ARGIPRESSIN;
ARGIPRESSIN RECEPTOR;
ARGIPRESSIN RECEPTOR 2;
UNCLASSIFIED DRUG;
ARTICLE;
BASE PAIRING;
CENTRAL DIABETES INSIPIDUS;
CHROMOSOME 20;
DIABETES INSIPIDUS;
GENE IDENTIFICATION;
GENETIC ANALYSIS;
GENOMICS;
HUMAN;
MEDICAL RESEARCH;
PHYSIOGENOMICS;
RISK FACTOR;
X CHROMOSOME;
ARGININE VASOPRESSIN;
CHROMOSOMES, HUMAN, PAIR 20;
CHROMOSOMES, HUMAN, X;
DIABETES INSIPIDUS, NEUROGENIC;
HUMANS;
RECEPTORS, VASOPRESSIN;
1
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Physiognomic perception: Empirical and theoretical perspectives
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Molecular diagnostics in endocrine diseases
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Current perspective on the pathogenesis of central diabetes insipidus
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The metabolic syndrome: Review of current concepts
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Application of chromosomal substitution techniques in gene-function discovery
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Consomic rat model systems for physiological genomics
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Physiogenomic resources for rat models of heart, lung and blood disorders
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8
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Diabetes insipidus
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10
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Repaske DR, Phillips JA 3rd. The molecular biology of human hereditary central diabetes insipidus. Prog Brain Res 1992;93:295-306.
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11
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Molecular biology of hereditary diabetes insipidus
Fujiwara TM, Bichet DG. Molecular biology of hereditary diabetes insipidus. J Am Soc Nephrol 2005;16:2836-46.
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Nephrogenic diabetes insipidus
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14
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Autosomal dominant familial neurohypophyseal diabetes insipidus
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Christensen, J.H.1
Siggaard, C.2
Rittig, S.3
15
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Non-syndromic progressive hearing loss DFNA38 is caused by heterozygous mis-sense mutation in the Wolfram syndrome gene WFS1
Young TL, Ives E, Lynch E, et al. Non-syndromic progressive hearing loss DFNA38 is caused by heterozygous mis-sense mutation in the Wolfram syndrome gene WFS1. Hum Mol Genet 2001;10:2509-14.
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Young, T.L.1
Ives, E.2
Lynch, E.3
16
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Glu-47, which forms a salt bridge between neurophysin-II and arginine vasopressin, is deleted in patients with familial central diabetes insipidus
Yuasa H, Ito M, Nagasaki H, et al. Glu-47, which forms a salt bridge between neurophysin-II and arginine vasopressin, is deleted in patients with familial central diabetes insipidus. J Clin Endocrinol Metab 1993;77:600-4.
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Yuasa, H.1
Ito, M.2
Nagasaki, H.3