| Expression analysis of a novel p75(NTR) signaling protein, which regulates cell cycle progression and apoptosis. | |
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MedLine Citation:
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PMID: 12204258 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neurotrophin receptor-interacting MAGE (NRAGE) is the most recently identified p75 neurotrophin receptor (p75(NTR)) intracellular binding protein. Previously, NRAGE over-expression was shown to mediate cell cycle arrest and facilitate nerve growth factor (NGF) dependent apoptosis of sympathetic neuroblasts in a p75(NTR) specific manner. Here we have examined the temporal and spatial expression patterns of NRAGE over the course of murine embryogenesis to determine whether NRAGE's expression is consistent with its proposed functions. We demonstrate that NRAGE mRNA and protein are expressed throughout embryonic and adult tissues. The mRNA is constitutively expressed within each tissue across development. However, expression of NRAGE protein displays a tight temporal tissue specific regulation. During early CNS development, NRAGE protein is expressed throughout the neural tube, but by later stages of neurogenesis, NRAGE protein is restricted within the ventricular zone, subplate and cortical plate. Moreover, NRAGE protein expression is limited to proliferative neural subpopulations as we fail to detect NRAGE expression co-localized with mature/differentiation associated neuronal markers. Interestingly, NRAGE's expression is not restricted solely to areas of p75(NTR) expression suggesting that NRAGE may mediate proliferation and/or apoptosis from other environmental signals in addition to NGF within the CNS. Our data support previously characterized roles for NRAGE as a mediator of precursor apoptosis and a repressor of cell cycle progression in neural development. |
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Authors:
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Stephen E Kendall; Donna E Goldhawk; Chris Kubu; Philip A Barker; Joseph M Verdi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Mechanisms of development Volume: 117 ISSN: 0925-4773 ISO Abbreviation: Mech. Dev. Publication Date: 2002 Sep |
Date Detail:
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Created Date: 2002-09-02 Completed Date: 2003-04-09 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9101218 Medline TA: Mech Dev Country: Ireland |
Other Details:
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Languages: eng Pagination: 187-200 Citation Subset: IM |
Copyright Information:
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Copyright 2002 Elsevier Science Ireland Ltd. |
Affiliation:
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The Laboratory of Neural Stem Cell Biology, The John P Robarts Research Institute, 100 Perth Drive, London, Ontario, Canada N6A 5K8. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antigens, Neoplasm Apoptosis / genetics, physiology* Base Sequence Cell Cycle / genetics, physiology* DNA-Binding Proteins / genetics*, metabolism* Gene Expression Regulation, Developmental Humans Mice Neoplasm Proteins* Nervous System / embryology, growth & development, metabolism Neurons / cytology, metabolism RNA, Messenger / genetics, metabolism Rats Receptor, Nerve Growth Factor Receptors, Nerve Growth Factor / metabolism* Signal Transduction Species Specificity Tissue Distribution |
| Chemical | |
Reg. No./Substance:
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0/Antigens, Neoplasm; 0/DNA-Binding Proteins; 0/MAGED1 protein, human; 0/Maged1 protein, mouse; 0/Maged1 protein, rat; 0/Neoplasm Proteins; 0/RNA, Messenger; 0/Receptor, Nerve Growth Factor; 0/Receptors, Nerve Growth Factor |
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