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2004 - Phoenix
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Peter van der Sluijs
Title:
MD
Email:
Phone:
Work ++31 30 250-7574, Work ++31 30 250-7578, Fax ++31 30 254-1797
Organization:
Utrecht University
Division:
School of Medicine
Department:
Department of Cell Biology
Address:
AZU Room G02.525 Heidelberglaan 100
3584 CX Utrecht,
Netherlands
6 Articles
6 Articles
Short-Chain Ubiquitination Mediates the Regulated Endocytosis of the Aquaporin-2 Water Channel
A Novel Mechanism in Recessive Nephrogenic Diabetes Insipidus: Wild-Type Aquaporin-2 Rescues the Apical Membrane Expression of Intracellularly Retained AQP2-P262L
Glycosylation is Important for Cell Surface Expression of the Water Channel Aquaporin-2, But is Not Essential for Tetramerization in the Endoplasmic Reticulum
Role of the Cytoplasmic Termini in the Sorting and Shuttling of the Aquaporin-2 Water Channel
The Role of Putative Phosphorylation Sites in the Targeting and Shuttling of the Aquaporin-2 Water Channel
An Aquaporin-2 Water Channel Mutant Which Causes Autosomal Dominant Nephrogenic Diabetes Insipidus is Retained in the Golgi Complex
6 Conference Proceedings
6 Conference Proceedings
Molecular mechanisms underlying dominant Nephrogenic Diabetes Insipidus caused by mutations in the AQP2 gene
Role of phosphorylation in the trafficking and shuttling of the Aquaporin-2 water channel
Impaired routing of AQP2 to late endosomes/lysosomes following heterotetramerization with AQP2-E258K is likely to explain dominant nephrogenic diabetes insipidus
N-linked glycosylation is essential for transport of the Aquaporin-2 water channel to the plasma membrane in MDCK cells
Mono-ubiquitination and missorting to lysosomes of the Aquaporin-2 water channel mutant AQP2-E258K explains dominant Nephrogenic Diabetes Insipidus
The novel Aquaporin-2 maturing protein 1 interacts with AQP2, inhibits its forskolin-induced translocation to the apical membrane, and reduces its expression
6 Articles
6 Articles