Document Detail

PTEN in neural precursor cells: regulation of migration, apoptosis, and proliferation.
MedLine Citation:
PMID:  12056837     Owner:  NLM     Status:  MEDLINE    
PTEN is a lipid phosphatase, and PTEN mutations are associated with gliomas, macrocephaly, and mental deficiencies. We have used PTEN +/- mice to assess PTEN's role in subventricular zone (SVZ) precursor cells. For cultured SVZ neurosphere cells, haploinsufficiency for PTEN increases phosphorylation of Akt and forkhead transcription factor and slightly enhances proliferation. Based on a filter penetration assay, PTEN +/- cells are substantially more migratory and invasive than +/+ cells. The +/- cells also are more resistant to H(2)O(2)-induced apoptosis. Analysis of PTEN +/- and +/+ mice by BrdU labeling reveals no difference in the rate of cell proliferation in the SVZ. Exit of BrdU-labeled cells from the SVZ and radial migration to the outer layers of the olfactory bulb are more rapid for +/- cells. These observations indicate that PTEN regulates SVZ precursor cell function and is particularly important for migration and apoptosis in response to oxidative stress.
Li Li; Fenghua Liu; Rebecca A Salmonsen; Tod K Turner; N Scott Litofsky; Antonio Di Cristofano; Pier Paolo Pandolfi; Stephen N Jones; Larry D Recht; Alonzo H Ross
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular and cellular neurosciences     Volume:  20     ISSN:  1044-7431     ISO Abbreviation:  Mol. Cell. Neurosci.     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-06-11     Completed Date:  2002-08-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9100095     Medline TA:  Mol Cell Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  21-9     Citation Subset:  IM    
Copyright Information:
(c) 2002 Elsevier Science (USA).
Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester 01605, USA.
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MeSH Terms
Apoptosis / physiology*
Brain / cytology,  growth & development*,  metabolism*
Bromodeoxyuridine / diagnostic use
Cell Count
Cell Division / physiology*
Cell Movement / physiology*
Cerebral Ventricles / cytology,  growth & development,  metabolism
Forkhead Transcription Factors
Mice, Knockout
Neurons / cytology,  metabolism*
Olfactory Bulb / cytology,  growth & development,  metabolism
Oxidative Stress / physiology
PTEN Phosphohydrolase
Phosphatidylinositol Phosphates / metabolism
Phosphoric Monoester Hydrolases / deficiency*,  genetics
Protein-Serine-Threonine Kinases*
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-akt
Stem Cells / cytology,  metabolism*
Transcription Factors / metabolism
Tumor Suppressor Proteins / deficiency*,  genetics
Grant Support
Reg. No./Substance:
0/Forkhead Transcription Factors; 0/Foxf1a protein, mouse; 0/Phosphatidylinositol Phosphates; 0/Proto-Oncogene Proteins; 0/Transcription Factors; 0/Tumor Suppressor Proteins; 0/phosphatidylinositol 3,4,5-triphosphate; 59-14-3/Bromodeoxyuridine; EC Kinases; EC Proteins c-akt; EC 3.1.3.-/Phosphoric Monoester Hydrolases; EC Phosphohydrolase

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