Source:http://linkedlifedata.com/resource/pubmed/id/17026715
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rdf:type | |
lifeskim:mentions |
umls-concept:C0010453,
umls-concept:C0035820,
umls-concept:C0037083,
umls-concept:C0109317,
umls-concept:C0596508,
umls-concept:C0752312,
umls-concept:C1150579,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1370600,
umls-concept:C1518294,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1710082
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pubmed:issue |
8
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pubmed:dateCreated |
2006-10-9
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pubmed:abstractText |
Embryonic stem (ES) cells represent an ideal source for cell engraftment in the damaged central nervous system (CNS). Understanding key signals that control ES cell differentiation may improve cell type-specific differentiation that is suitable for transplantation therapy. We tested the hypothesis that extracellular signal-regulated kinase (ERK) 1/2 phosphorylation is an early signaling event required for the neuronal differentiation of ES cells. Cultured mouse ES cells were treated with an all-trans-retinoic-acid (RA) protocol to generate neurally induced progenitor cells. Western blot analysis showed a dramatic increase in ERK 1/2 phosphorylation (p-ERK 1/2) 1-5 days after RA induction, which was attenuated in the presence of the p-ERK 1/2-specific inhibitor UO126. Phospho-ERK 1/2 inhibition significantly reduced the number of NeuN-positive cells and the expression of associated cytoskeletal proteins. In differentiating ES cells, there was increased nuclear translocation of STAT3 and decreased protein expression levels of GDNF, BDNF and NGF. STAT3 translocation was attenuated by UO126. Finally, caspase-3 activation was observed in the presence of UO126, suggesting that the ERK pathway also contributes to the survival of differentiating ES cells. These data indicate that ERK 1/2 phosphorylation is a key event required for early neuronal differentiation and survival of ES cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0012-1592
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
513-23
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17026715-Animals,
pubmed-meshheading:17026715-Antineoplastic Agents,
pubmed-meshheading:17026715-Cell Differentiation,
pubmed-meshheading:17026715-Cell Line,
pubmed-meshheading:17026715-Embryonic Stem Cells,
pubmed-meshheading:17026715-MAP Kinase Signaling System,
pubmed-meshheading:17026715-Mice,
pubmed-meshheading:17026715-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:17026715-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:17026715-Neurons,
pubmed-meshheading:17026715-Stem Cell Transplantation,
pubmed-meshheading:17026715-Tretinoin
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pubmed:year |
2006
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pubmed:articleTitle |
Role of ERK 1/2 signaling in neuronal differentiation of cultured embryonic stem cells.
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pubmed:affiliation |
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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