Cell Cycle Phase-Specific Surface Expression of Nerve Growth Factor Receptors TrkA and p75NTR

[EN]Expression of the nerve growth factor (NGF) receptors TrkA and p75NTR was found to vary at the surface of PC12 cells in a cell cycle phase-specific manner. This was evidenced by using flow cytometric and microscopic analysis of cell populations labeled with antibodies to the extracellular domain...

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Detalles Bibliográficos
Autores: Urdiales, José Luis, Becker, Elena, Andrieu, Muriel, Thomas, Annie, Jullien, Jérôme, van Grunsven, Leo A., Menut, Sophie, Evan, Gerard I., Martı́n-Zanca, Dionisio, Rudkin, Brian B.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:1998
País:España
Institución:Universidad de Salamanca (USAL)
Repositorio:GREDOS. Repositorio Institucional de la Universidad de Salamanca
OAI Identifier:oai:gredos.usal.es:10366/146279
Acceso en línea:http://hdl.handle.net/10366/146279
Access Level:acceso abierto
Palabra clave:Signaling
PC12 cells
TrkA antibodies
p75NTR antibodies
Flow cytometry
Cell cycle
Neurotrophin
Receptor
Cell Cycle
Receptor, trkA
2490 Neurociencias
ciclo celular
receptor trkA
Descripción
Sumario:[EN]Expression of the nerve growth factor (NGF) receptors TrkA and p75NTR was found to vary at the surface of PC12 cells in a cell cycle phase-specific manner. This was evidenced by using flow cytometric and microscopic analysis of cell populations labeled with antibodies to the extracellular domains of both receptors. Differential expression of these receptors also was evidenced by biotinylation of surface proteins and Western analysis, using antibodies specific for the extracellular domains of TrkA and p75NTR. TrkA is expressed most strongly at the cell surface in M and early G1 phases, whereas p75NTR is expressed mainly in late G1, S, and G2 phases. This expression reflects the molecular and cellular responses to NGF in specific phases of the cell cycle; in the G1 phase NGF elicits both the anti-mitogenic effect, i.e., inhibition of the G1 to S transition, and the differentiation response whereas a survival effect is provoked elsewhere in the cell cycle. A model is proposed relating these responses to the surface expression of the two receptors. These observations open the way for novel approaches to the investigation of the mechanism of NGF signal transduction.