Linked Life Data

15339978

Source:http://linkedlifedata.com/resource/pubmed/id/15339978

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-9-1
pubmed:abstractText
Podocalyxin (PC) is the major sialoglycoprotein expressed on the apical membrane of the podocyte. Previously it was shown that PC is connected to actin through the PC/NHERF2/ezrin complex, and this connection is disrupted in the nephrotic syndrome. For assessing whether expression of PC affects the organization of the actin cytoskeleton, MDCK cell lines stably expressing either full-length PC or a PC mutant lacking the NHERF binding site was established. It was found that full-length PC but not the PC mutant is connected to actin, induces redistribution of actin toward the apical membrane, and leads to increased RhoA activity. By immunofluorescence redistribution of RhoA and RhoGDI was observed in the presence of both full-length PC and the PC mutant. With the use of pulldown assays, PC and ezrin were found to interact directly and the ezrin binding site was mapped to the juxtamembrane region of PC's cytoplasmic tail. It is concluded that PC binds to ezrin both directly and indirectly. PC activates RhoA through NHERF and ezrin, leading to redistribution of actin filaments. These results suggest that in podocytes, PC may also regulate foot process architecture through RhoA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2289-98
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Podocalyxin activates RhoA and induces actin reorganization through NHERF1 and Ezrin in MDCK cells.
pubmed:affiliation
Department of Cellular and Molecular Medicine, George Palade Laboratories Room 210, 9500 Gilman Drive, La Jolla, CA 92093-0651, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't