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2004 - Phoenix
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Erik-Jan Kamsteeg
Title:
MD
Email:
Phone:
Work +1-31 24-361-0573, Fax +1-31 24-361-6413
Organization:
University of Nijmegen
Division:
160, Dept. of Cell Physiology
Address:
NCMLS Research Tower, 7th Floor UMC St Radboud P.O. Box 9101
6500 HB Nijmegen,
Netherlands
13 Articles
13 Articles
MAL Decreases the Internalization of the Aquaporin-2 Water Channel
Short-Chain Ubiquitination Mediates the Regulated Endocytosis of the Aquaporin-2 Water Channel
Development of Lithium-Induced Nephrogenic Diabetes Insipidus is Dissociated from Adenylyl Cyclase Activity
A Novel Mechanism in Recessive Nephrogenic Diabetes Insipidus: Wild-Type Aquaporin-2 Rescues the Apical Membrane Expression of Intracellularly Retained AQP2-P262L
Reversed Polarized Delivery of an Aquaporin-2 Mutant Causes Dominant Nephrogenic Diabetes Insipidus
Aquaporin-2: COOH Terminus is Necessary But Not Sufficient for Routing to the Apical Membrane
Detection of aquaporin-2 in the plasma membranes of oocytes: a novel isolation method with improved yield and purity.
Defective processing and trafficking of water channels in nephrogenic diabetes insipidus.
Importance of Aquaporin-2 Expression Levels in Genotype -Phenotype Studies in Nephrogenic Diabetes Insipidus
Physiological relevance of aquaporins: luxury or necessity?
Routing of the aquaporin-2 water channel in health and disease.
An Impaired Routing of Wild-type Aquaporin-2 after Tetramerization with an Aquaporin-2 Mutant Explains Dominant Nephrogenic Diabetes Insipidus
An Aquaporin-2 Water Channel Mutant Which Causes Autosomal Dominant Nephrogenic Diabetes Insipidus is Retained in the Golgi Complex
11 Conference Proceedings
11 Conference Proceedings
Determination of the functionality of AQP2 missense mutants in recessive NDI
The C-terminus of aquaporin-2 is necessary, but not sufficient, for routing of AQP2 to the apical membrane
An impaired routing of wild type aquaporin-2 after tetramerization with an aquaporin-2 mutant explains dominant nephrogenic diabetes insipidus
Consequences of tetramerization and expression levels of Aquaporin-2 in phenotype-genotype correlation studies in autosomal NDI
The stoichiometry of phosphorylated and non-phosphorylated monomers in an aquaporin-2 tetramer determines its subcellular localization
Molecular mechanisms underlying dominant Nephrogenic Diabetes Insipidus caused by mutations in the AQP2 gene
Impaired routing of AQP2 to late endosomes/lysosomes following heterotetramerization with AQP2-E258K is likely to explain dominant nephrogenic diabetes insipidus
Mono-ubiquitination and missorting to lysosomes of the Aquaporin-2 water channel mutant AQP2-E258K explains dominant Nephrogenic Diabetes Insipidus
Wild-type aquaporin-2 rescues a novel aquaporin-2 mutant in recessive Nephrogenic Diabetes Insipidus to the apical plasma membrane
The novel Aquaporin-2 maturing protein 1 interacts with AQP2, inhibits its forskolin-induced translocation to the apical membrane, and reduces its expression
Lithium-induced Nephrogenic Diabetes Insipidus: A Cell Culture Model
13 Articles
13 Articles