Linked Life Data

16508302

Source:http://linkedlifedata.com/resource/pubmed/id/16508302

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2006-3-1
pubmed:abstractText
Recently, Notch signaling has been reported to underscore the ability of neural stem cells (NSCs) to self-renew. Utilizing mice deficient in presenilin-1(PS1), we asked whether the function of Notch signaling in NSC maintenance was conserved. At embryonic day 14.5, all NSCs--both similar (cortex-, ganglionic eminence- and hindbrain-derived) and distinct (retinal stem cell)--require Notch signaling in a gene-dosage-sensitive manner to undergo expansionary symmetric divisions, as assessed by the clonal, in vitro neurosphere assay. Within the adult, however, Notch signaling modulates cell cycle time in order to ensure brain-derived NSCs retain their self-renewal property. At face value, the effects in the embryo and adult appear different. We propose potential hypotheses, including the ability of cell cycle to modify the mode of division, in order to resolve this discrepancy. Regardless, these findings demonstrate that PS1, and presumably Notch signaling, is required to maintain all NSCs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0378-5866
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2006 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
34-48
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Notch signaling is required to maintain all neural stem cell populations--irrespective of spatial or temporal niche.
pubmed:affiliation
Neurobiology Research Group, Department of Medical Biophysics, University of Toronto, Toronto, Canada. talexson@thinkers.cx
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't