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dc.contributor.author
Sánchez Jiménez, Flora
dc.contributor.author
Pérez Pérez, Antonio
dc.contributor.author
González Yanes, Carmen
dc.contributor.author
Najib, Souad
dc.contributor.author
Varone, Cecilia Laura
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dc.contributor.author
Sánchez Margalet, Víctor
dc.date.available
2020-01-27T19:21:14Z
dc.date.issued
2011-01
dc.identifier.citation
Sánchez Jiménez, Flora; Pérez Pérez, Antonio; González Yanes, Carmen; Najib, Souad; Varone, Cecilia Laura; et al.; Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells; Elsevier Ireland; Molecular and Cellular Endocrinology; 332; 1-2; 1-2011; 221-227
dc.identifier.issn
0303-7207
dc.identifier.uri
http://hdl.handle.net/11336/95881
dc.description.abstract
Leptin is produced in placenta where it has been found to be an important autocrine signal for trophoblastic growth during pregnancy, promoting antiapoptotic and trophic effects. Leptin receptor is present in trophoblastic cells and leptin may fully activate signaling. We have previously implicated the RNA-binding protein Sam68 in leptin signal transduction in immune cells. In the present work, we have studied the possible role of Sam68 in leptin receptor signaling in trophoblastic cells (JEG-3 cells). Leptin dose-dependently stimulated Sam68 phosphorylation in JEG-3 cells, as assessed by immunoprecipitation and immunoblot with anti-phosphotyrosine antibodies. As previously observed in other systems, tyrosine phosphorylation of Sam68 in response to leptin inhibits its RNA binding capacity. Besides, leptin stimulation dose-dependently increases Sam68 expression in JEG-3 cells, as assessed by quantitative PCR. Consistently, the amount of Sam68 protein is increased after 24. h of leptin stimulation of trophoblastic cells. In order to study the possible role of Sam68 on leptin receptor synthesis, we employed antisense strategy to knockdown the expression of Sam68. We have found that a decrease in Sam68 expression leads to a decrease in leptin receptor amount in JEG-3 cells, as assessed both by quantitative PCR and immunoblot.These results strongly suggest the participation of Sam68 in leptin receptor signaling in human trophoblastic cells, and therefore, Sam68 may mediate some of the leptin effects in placenta.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Ireland
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
LEPTIN RECEPTOR
dc.subject
PLACENTA
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SAM68
dc.subject
SIGNAL TRANSDUCTION
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Leptin receptor activation increases Sam68 tyrosine phosphorylation and expression in human trophoblastic cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-11-08T15:09:15Z
dc.journal.volume
332
dc.journal.number
1-2
dc.journal.pagination
221-227
dc.journal.pais
Irlanda
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dc.journal.ciudad
Amsterdam
dc.description.fil
Fil: Sánchez Jiménez, Flora. Hospital Universitario Virgen Macarena; España
dc.description.fil
Fil: Pérez Pérez, Antonio. Hospital Universitario Virgen Macarena; España
dc.description.fil
Fil: González Yanes, Carmen. Hospital Universitario Virgen Macarena; España
dc.description.fil
Fil: Najib, Souad. Institut de Médecine Moléculaire de Rangueil; Francia
dc.description.fil
Fil: Varone, Cecilia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
dc.description.fil
Fil: Sánchez Margalet, Víctor. Hospital Universitario Virgen Macarena; España
dc.journal.title
Molecular and Cellular Endocrinology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0303720710005022
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1016/j.mce.2010.10.014
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