Expression of milk protein genes is induced directly by exogenous STAT5 without prolactin-mediated signal transduction in transgenic mice

STAT5 is a member of the family of STAT (signal transducer for activating transcription), which was isolated from nuclear extracts of the lactating gland of sheep. It was reported that, in vitro, STAT5 could be activated directly by prolactin (PRL) without PRL‐mediated signal transduction. The prese...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Molecular reproduction and development 1999-10, Vol.54 (2), p.121-125
Hauptverfasser: Inuzuka, H, Yamanouchi, K, Tachi, C, Tojo, H
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:STAT5 is a member of the family of STAT (signal transducer for activating transcription), which was isolated from nuclear extracts of the lactating gland of sheep. It was reported that, in vitro, STAT5 could be activated directly by prolactin (PRL) without PRL‐mediated signal transduction. The present study was conducted to investigate above the possibility in vivo, using the transgenic mice overexpressing ovine STAT5 (oSTAT5) under the control of MMTV promoter. Three transgenic mouse lines that expressed the exogenously introduced oSTAT5 in their mammary glands were established. The expression levels of exogenous oSTAT5 were higher than those of endogenous STAT in the mammary glands of all of the three transgenic lines. Although the expression levels of endogenous milk protein genes, WAP, and β‐casein genes, were not correlated with oSTAT5 expression, the expression levels of WAP and β‐casein were induced by exogenous oSTAT5 in the transgenic mice. The present study demonstrated, at very least, that STAT5 expression can directly activate the expression of milk protein genes, and particularly the WAP gene without PRL‐mediated signal transduction. Mol. Reprod. Dev. 54:121–125, 1999. © 1999 Wiley‐Liss, Inc.
ISSN:1040-452X
1098-2795
DOI:10.1002/(SICI)1098-2795(199910)54:2<121::AID-MRD3>3.0.CO;2-T