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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
21
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pubmed:dateCreated |
2011-5-23
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pubmed:abstractText |
Murine SEL-1L (mSEL-1L) is a key component of the endoplasmic reticulum-associated degradation pathway. It is essential during development as revealed by the multi-organ dysfunction and in uterus lethality occurring in homozygous mSEL-1L-deficient mice. Here we show that mSEL-1L is highly expressed in pluripotent embryonic stem cells and multipotent neural stem cells (NSCs) but silenced in all mature neural derivatives (i.e. astrocytes, oligodendrocytes, and neurons) by mmu-miR-183. NSCs derived from homozygous mSEL-1L-deficient embryos (mSEL-1L(-/-) NSCs) fail to proliferate in vitro, show a drastic reduction of the Notch effector HES-5, and reveal a significant down-modulation of the early neural progenitor markers PAX-6 and OLIG-2, when compared with the wild type (mSEL-1L(+/+) NSCs) counterpart. Furthermore, these cells are almost completely deprived of the neural marker Nestin, display a significant decrease of SOX-2 expression, and rapidly undergo premature astrocytic commitment and apoptosis. The data suggest severe self-renewal defects occurring in these cells probably mediated by misregulation of the Notch signaling. The results reported here denote mSEL-1L as a primitive marker with a possible involvement in the regulation of neural progenitor stemness maintenance and lineage determination.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix...,
http://linkedlifedata.com/resource/pubmed/chemical/Eye Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Hes5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Intermediate Filament Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/MicroRNAs,
http://linkedlifedata.com/resource/pubmed/chemical/Mirn183 microRNA, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Olig2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/PAX6 protein,
http://linkedlifedata.com/resource/pubmed/chemical/Paired Box Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Sel1h protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/nestin
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1083-351X
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
27
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
18708-19
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pubmed:meshHeading |
pubmed-meshheading:21454627-Animals,
pubmed-meshheading:21454627-Antigens, Differentiation,
pubmed-meshheading:21454627-Apoptosis,
pubmed-meshheading:21454627-Astrocytes,
pubmed-meshheading:21454627-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:21454627-Cell Line,
pubmed-meshheading:21454627-Cell Lineage,
pubmed-meshheading:21454627-Eye Proteins,
pubmed-meshheading:21454627-Homeodomain Proteins,
pubmed-meshheading:21454627-Intermediate Filament Proteins,
pubmed-meshheading:21454627-Mice,
pubmed-meshheading:21454627-Mice, Transgenic,
pubmed-meshheading:21454627-MicroRNAs,
pubmed-meshheading:21454627-Multipotent Stem Cells,
pubmed-meshheading:21454627-Nerve Tissue Proteins,
pubmed-meshheading:21454627-Neural Stem Cells,
pubmed-meshheading:21454627-Paired Box Transcription Factors,
pubmed-meshheading:21454627-Proteins,
pubmed-meshheading:21454627-Repressor Proteins
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pubmed:year |
2011
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pubmed:articleTitle |
mSEL-1L (Suppressor/enhancer Lin12-like) protein levels influence murine neural stem cell self-renewal and lineage commitment.
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pubmed:affiliation |
Doctorate School of Molecular Medicine, Università degli Studi di Milano, 20100 Milan, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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