Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2000-10-5
pubmed:abstractText
We have discovered that intracellular redox state appears to be a necessary and sufficient modulator of the balance between self-renewal and differentiation in dividing oligodendrocyte-type-2 astrocyte progenitor cells. The intracellular redox state of freshly isolated progenitors allows prospective isolation of cells with different self-renewal characteristics. Redox state is itself modulated by cell-extrinsic signaling molecules that alter the balance between self-renewal and differentiation: growth factors that promote self-renewal cause progenitors to become more reduced, while signaling molecules that promote differentiation cause progenitors to become more oxidized. Moreover, pharmacological antagonists of the redox effects of these cell-extrinsic signaling molecules antagonize their effects on self-renewal and differentiation, indicating that cell-extrinsic signaling molecules that modulate this balance converge on redox modulation as a critical component of their effector mechanism.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-10075689, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-10206339, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-1537340, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-1681551, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2018489, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2023917, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2201028, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2648959, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2834067, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-2865163, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3287176, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3287177, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3536548, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3656363, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3722629, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-388422, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-3948247, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-4559710, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-6137189, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-6304520, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-6542000, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-6586375, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-7006734, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-7045870, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-7513425, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-7914368, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8026323, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8114937, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8215909, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8375338, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8464477, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-8948570, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9029151, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9034240, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9100544, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9130244, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9151728, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9183012, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9308962, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9361279, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9406919, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9550698, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9596656, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9733077, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9796694, http://linkedlifedata.com/resource/pubmed/commentcorrection/10944195-9928441
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10032-7
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Redox state is a central modulator of the balance between self-renewal and differentiation in a dividing glial precursor cell.
pubmed:affiliation
Huntsman Cancer Institute, Department of Oncological Sciences, University of Utah, 2000 N. Medical Drive, Room 4280, Salt Lake City, UT 84112, USA.
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