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c‐myc as a mediator of accelerated apoptosis and involution in mammary glands lacking Socs3

Identifieur interne : 000668 ( Main/Exploration ); précédent : 000667; suivant : 000669

c‐myc as a mediator of accelerated apoptosis and involution in mammary glands lacking Socs3

Auteurs : Kate D. Sutherland [Australie] ; François Vaillant [Australie] ; Warren S. Alexander [Australie] ; Tim M. Wintermantel [Allemagne] ; Natasha C. Forrest [Australie] ; Sheridan L. Holroyd [Australie] ; Edward J. Mcmanus [Australie] ; Gunther Schutz [Allemagne] ; Christine J. Watson [Royaume-Uni] ; Lewis A. Chodosh [États-Unis] ; Geoffrey J. Lindeman [Australie] ; Jane E. Visvader [Australie]

Source :

RBID : ISTEX:5114DB92A5B5DE1FD2034F458D263A91BCCE4813

Abstract

Suppressor of cytokine signalling (SOCS) proteins are critical attenuators of cytokine‐mediated signalling in diverse tissues. To determine the importance of Socs3 in mammary development, we generated mice in which Socs3 was deleted in mammary epithelial cells. No overt phenotype was evident during pregnancy and lactation, indicating that Socs3 is not a key physiological regulator of prolactin signalling. However, Socs3‐deficient mammary glands exhibited a profound increase in epithelial apoptosis and tissue remodelling, resulting in precocious involution. This phenotype was accompanied by augmented Stat3 activation and a marked increase in the level of c‐myc. Moreover, induction of c‐myc before weaning using an inducible transgenic model recapitulated the Socs3 phenotype, and elevated expression of likely c‐myc target genes, E2F‐1, Bax and p53, was observed. Our data establish Socs3 as a critical attenuator of pro‐apoptotic pathways that act in the developing mammary gland and provide evidence that c‐myc regulates apoptosis during involution.


Url:
DOI: 10.1038/sj.emboj.7601455


Affiliations:


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Le document en format XML

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