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Characterization of NADE, NRIF and SC-1 gene expression during mouse neurogenesis
The p75 neurotrophin receptor (p75 NTR) is a member of the tumor necrosis factor receptor superfamily. p75 NTR signaling events have been implicated in both cell cycle arrest and apoptosis depending on which effector molecules are associated with its intracellular domain after ligand binding. Two su...
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Published in: | Brain research. Developmental brain research 2003-09, Vol.144 (2), p.151-158 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The p75 neurotrophin receptor (p75
NTR) is a member of the tumor necrosis factor receptor superfamily. p75
NTR signaling events have been implicated in both cell cycle arrest and apoptosis depending on which effector molecules are associated with its intracellular domain after ligand binding. Two such effector proteins, p75
NTR-associated cell death executor (NADE) and neurotrophin receptor interacting factor (NRIF) promote p75
NTR-mediated apoptosis, whereas Schwann cell factor-1 (SC-1) mediates neurotrophin-dependent withdrawal from the cell cycle. An understanding of the expression profiles of these three interacting proteins and p75
NTR during embryogenesis is critical for addressing whether these effector proteins might function outside of p75
NTR-mediated signaling events. The distribution of NADE, NRIF and SC-1 mRNAs during murine development suggests that the action of these genes is in fact not limited to regions of p75
NTR expression. Specifically, a detailed comparison of the spatial and temporal expression domains of NADE, NRIF and SC-1 during brain development revealed regions of co-expression with p75
NTR but also illustrates a distinct and discordant spatial and temporal expression. These results yield novel insights into the unique developmental characteristics of the three p75
NTR-interacting proteins, thus revealing their diverse signaling potential during embryonic development. |
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ISSN: | 0165-3806 |
DOI: | 10.1016/S0165-3806(03)00166-4 |