| http://purl.uniprot.org/citations/24064341 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24064341 | http://www.w3.org/2000/01/rdf-schema#comment | "Prolactin (PRL) and placental lactogens stimulate β-cell replication and insulin production in pancreatic islets and insulinoma cells through binding to the PRL receptor (PRLR). However, the contribution of PRLR signaling to β-cell ontogeny and function in perinatal life and the effects of the lactogens on adaptive islet growth are poorly understood. We provide evidence that expansion of β-cell mass during both embryogenesis and the postnatal period is impaired in the PRLR(-/-) mouse model. PRLR(-/-) newborns display a 30% reduction of β-cell mass, consistent with reduced proliferation index at E18.5. PRL stimulates leucine incorporation and S6 kinase phosphorylation in INS-1 cells, supporting a role for β-cell mTOR signaling in PRL action. Interestingly, a defect in the development of acini is also observed in absence of PRLR signaling, with a sharp decline in cellular size in both endocrine and exocrine compartments. Of note, a decrease in levels of IGF-II, a PRL target, in the Goto-Kakizaki (GK) rat, a spontaneous model of type 2 diabetes, is associated with a lack of PRL-mediated β-cell proliferation in embryonic pancreatic buds. Reduced pancreatic IGF-II expression in both rat and mouse models suggests that this factor may constitute a molecular link between PRL signaling and cell ontogenesis. Together, these results provide evidence that PRL signaling is essential for pancreas ontogenesis during the critical perinatal window responsible for establishing functional β-cell reserve."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpendo.00636.2012"xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Binart N."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Mathieu Y."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Lombes M."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Freemark M."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Movassat J."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Tourrel-Cuzin C."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Carre N."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/author | "Auffret J."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/name | "Am J Physiol Endocrinol Metab"xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/pages | "E1309-18"xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/title | "Defective prolactin signaling impairs pancreatic beta-cell development during the perinatal period."xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://purl.uniprot.org/core/volume | "305"xsd:string |
| http://purl.uniprot.org/citations/24064341 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24064341 |
| http://purl.uniprot.org/citations/24064341 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24064341 |
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| http://purl.uniprot.org/uniprot/#_E9Q0U8-mappedCitation-24064341 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24064341 |
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| http://purl.uniprot.org/uniprot/#_A2AS86-mappedCitation-24064341 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24064341 |