Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-1-13
pubmed:abstractText
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) are caused by mutations of the TAU gene. Many such mutations are located near the splicing site of exon 10 and affect the splicing ratio of 3-repeat/4-repeat tau isoforms (referred to as 3R-tau and 4R-tau) which contain 3 and 4 microtubule-binding domains, respectively. Little is known, however, concerning cellular localization of 3R-tau and 4R-tau. We examined the subcellular localization of tau isoforms in IMR-32 cells under differentiated conditions using the fusion proteins of tau isoforms probed with fluorescent protein (EGFP). 3R-tau was observed in spotty and rarely linear distributions while 4R-tau was observed in linear and sometimes spotty distributions. Together with findings of phase-contrast microscopy of cultured cells, these results indicated that 3R- and 4R-tau were predominantly localized at growth tips/branching points and along neurite processes, respectively. Due to their different localizations, balanced expression of 3R- and 4R-tau may coordinate plastic morphogenesis and stabilization of neurite processes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0030-6096
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19-27
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The distributions of tau short and long isoforms fused with EGFP in cultured cells.
pubmed:affiliation
Department of Neuroscience, Osaka City University Medical School, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't