| Nephrin-signature molecule of the glomerular podocyte? | |
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MedLine Citation:
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PMID: 19950250 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In recent years there has been an explosion of interest in the glomerular podocyte, which plays a central role in control of glomerular filtration. A host of new molecules have been identified as playing essential roles in the maintenance of podocyte integrity in both humans and mouse models. Of all of these, arguably the most pivotal is nephrin, a transmembrane receptor molecule located at the specialized podocyte cell-cell junction, termed the slit diaphragm. Mutations in this gene cause the most severe form of congenital nephrotic syndrome, and many interacting proteins have now been described to form a large multiprotein complex with complex dynamics. There is little evidence of functional nephrin expression outside the glomerulus, and there are accumulating data that nephrin is essential for the unique properties of podocyte biology. Utilizing a powerful human cell culture model, comparing wild-type with nephrin-null podocytes, we can show that several crucial functional properties of podocytes depend on nephrin, including insulin responsiveness and cytoskeletal reorganization. Thus, it is reasoned that nephrin is a signature molecule required to define distinct podocyte characteristics. |
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Authors:
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Gavin I Welsh; Moin A Saleem |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: The Journal of pathology Volume: 220 ISSN: 1096-9896 ISO Abbreviation: J. Pathol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-02-01 Completed Date: 2010-03-26 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0204634 Medline TA: J Pathol Country: England |
Other Details:
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Languages: eng Pagination: 328-37 Citation Subset: IM |
Copyright Information:
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Copyright 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
Affiliation:
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University of Bristol, Children's Renal Unit, Bristol Royal Hospital for Children, UK. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Diabetic Nephropathies / physiopathology Genotype Humans Kidney Glomerulus / physiology Membrane Proteins / genetics, physiology* Mice Mutation Nephrotic Syndrome / metabolism Phenotype Podocytes / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Membrane Proteins; 0/nephrin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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