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From the molecular biology of prolactin and its receptor to the lessons learned from knockout mice models

Identifieur interne : 00C521 ( Main/Exploration ); précédent : 00C520; suivant : 00C522

From the molecular biology of prolactin and its receptor to the lessons learned from knockout mice models

Auteurs : Vincent Goffin [France] ; Nadine Binart [France] ; Philippe Clément-Lacroix [France] ; Brigitte Bouchard [France] ; Christine Bole-Feysot [France] ; Marc Edery [France] ; Brian K. Lucas [France] ; Philippe Touraine [France] ; Alain Pezet [France] ; Ronda Maaskant [France] ; Caroline Pichard [France] ; Christine Helloco [France] ; Nathalie Baran [France] ; Hélène Favre [France] ; Sophie Bernichtein [France] ; Angélique Allamando [France] ; Christopher Ormandy [Australie] ; Paul A. Kelly [France]

Source :

RBID : ISTEX:FDAAD7E1C97C754BA8A97A51BC8DE057744D44C6

English descriptors

Abstract

Abstract: Prolactin (PRL), a polypeptide hormone secreted mainly by the pituitary and, to a lesser extent, by peripheral tissues, affects more physiological processes than all other pituitary hormones combined since it is involved in>300 separate functions in vertebrates. Its main actions are related to lactation and reproduction. The initial step of PRL action is the binding to a specific membrane receptor, the PRLR, which belongs to the class 1 cytokine receptor superfamily. PRL-binding sites have been identified in a number of tissues and cell types in adult animals. Signal transduction by this receptor is mediated, at least in part, by two families of signaling molecules: Janus tyrosine kinases and signal transducers and activators of transcription (STATs). Disruption of the PRLR gene has provided a new mouse model with which to identify actions directly associated with PRL or any other PRLR ligands, such as placental lactogens. To date, several different phenotypes have been analyzed and are briefly described in this review. Coupled with the SAGE technique, this PRLR knockout model is being used to qualitatively and quantitatively evaluate the expression pattern of hepatic genes in two physiological situations: transcriptomes corresponding to livers from both wild type and PRLR KO mice are being compared, and following statistical analyses, candidate genes presenting a differential profile will be further characterized. Such a new approach will undoubtedly open future avenues of research for PRL targets. To date, no pathology linked to any mutation in the genes encoding PRL or its receptor have been identified. The development of genetic models provides new opportunities to understand how PRL can participate to the development of pathologies throughout life, as for example the initiation and progression of breast cancer.

Url:
DOI: 10.1016/S1050-3862(99)00025-X


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<div type="abstract" xml:lang="en">Abstract: Prolactin (PRL), a polypeptide hormone secreted mainly by the pituitary and, to a lesser extent, by peripheral tissues, affects more physiological processes than all other pituitary hormones combined since it is involved in>300 separate functions in vertebrates. Its main actions are related to lactation and reproduction. The initial step of PRL action is the binding to a specific membrane receptor, the PRLR, which belongs to the class 1 cytokine receptor superfamily. PRL-binding sites have been identified in a number of tissues and cell types in adult animals. Signal transduction by this receptor is mediated, at least in part, by two families of signaling molecules: Janus tyrosine kinases and signal transducers and activators of transcription (STATs). Disruption of the PRLR gene has provided a new mouse model with which to identify actions directly associated with PRL or any other PRLR ligands, such as placental lactogens. To date, several different phenotypes have been analyzed and are briefly described in this review. Coupled with the SAGE technique, this PRLR knockout model is being used to qualitatively and quantitatively evaluate the expression pattern of hepatic genes in two physiological situations: transcriptomes corresponding to livers from both wild type and PRLR KO mice are being compared, and following statistical analyses, candidate genes presenting a differential profile will be further characterized. Such a new approach will undoubtedly open future avenues of research for PRL targets. To date, no pathology linked to any mutation in the genes encoding PRL or its receptor have been identified. The development of genetic models provides new opportunities to understand how PRL can participate to the development of pathologies throughout life, as for example the initiation and progression of breast cancer.</div>
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<name sortKey="Baran, Nathalie" sort="Baran, Nathalie" uniqKey="Baran N" first="Nathalie" last="Baran">Nathalie Baran</name>
<name sortKey="Bernichtein, Sophie" sort="Bernichtein, Sophie" uniqKey="Bernichtein S" first="Sophie" last="Bernichtein">Sophie Bernichtein</name>
<name sortKey="Binart, Nadine" sort="Binart, Nadine" uniqKey="Binart N" first="Nadine" last="Binart">Nadine Binart</name>
<name sortKey="Bole Feysot, Christine" sort="Bole Feysot, Christine" uniqKey="Bole Feysot C" first="Christine" last="Bole-Feysot">Christine Bole-Feysot</name>
<name sortKey="Bouchard, Brigitte" sort="Bouchard, Brigitte" uniqKey="Bouchard B" first="Brigitte" last="Bouchard">Brigitte Bouchard</name>
<name sortKey="Clement Lacroix, Philippe" sort="Clement Lacroix, Philippe" uniqKey="Clement Lacroix P" first="Philippe" last="Clément-Lacroix">Philippe Clément-Lacroix</name>
<name sortKey="Edery, Marc" sort="Edery, Marc" uniqKey="Edery M" first="Marc" last="Edery">Marc Edery</name>
<name sortKey="Favre, Helene" sort="Favre, Helene" uniqKey="Favre H" first="Hélène" last="Favre">Hélène Favre</name>
<name sortKey="Goffin, Vincent" sort="Goffin, Vincent" uniqKey="Goffin V" first="Vincent" last="Goffin">Vincent Goffin</name>
<name sortKey="Helloco, Christine" sort="Helloco, Christine" uniqKey="Helloco C" first="Christine" last="Helloco">Christine Helloco</name>
<name sortKey="Kelly, Paul A" sort="Kelly, Paul A" uniqKey="Kelly P" first="Paul A" last="Kelly">Paul A. Kelly</name>
<name sortKey="Lucas, Brian K" sort="Lucas, Brian K" uniqKey="Lucas B" first="Brian K" last="Lucas">Brian K. Lucas</name>
<name sortKey="Maaskant, Ronda" sort="Maaskant, Ronda" uniqKey="Maaskant R" first="Ronda" last="Maaskant">Ronda Maaskant</name>
<name sortKey="Pezet, Alain" sort="Pezet, Alain" uniqKey="Pezet A" first="Alain" last="Pezet">Alain Pezet</name>
<name sortKey="Pichard, Caroline" sort="Pichard, Caroline" uniqKey="Pichard C" first="Caroline" last="Pichard">Caroline Pichard</name>
<name sortKey="Touraine, Philippe" sort="Touraine, Philippe" uniqKey="Touraine P" first="Philippe" last="Touraine">Philippe Touraine</name>
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<country name="Australie">
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<name sortKey="Ormandy, Christopher" sort="Ormandy, Christopher" uniqKey="Ormandy C" first="Christopher" last="Ormandy">Christopher Ormandy</name>
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