c‐myc as a mediator of accelerated apoptosis and involution in mammary glands lacking Socs3
Identifieur interne : 000658 ( Main/Exploration ); précédent : 000657; suivant : 000659c‐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 :
- The EMBO Journal [ 0261-4189 ] ; 2006-12-13.
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:
- Allemagne, Australie, Royaume-Uni, États-Unis
- Angleterre, Angleterre de l'Est, Bade-Wurtemberg, District de Karlsruhe, Pennsylvanie, Victoria (État)
- Cambridge, Heidelberg, Melbourne, Philadelphie
- Université de Cambridge, Université de Melbourne
Links toward previous steps (curation, corpus...)
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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.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Bade-Wurtemberg</li><li>District de Karlsruhe</li><li>Pennsylvanie</li><li>Victoria (État)</li></region><settlement><li>Cambridge</li><li>Heidelberg</li><li>Melbourne</li><li>Philadelphie</li></settlement><orgName><li>Université de Cambridge</li><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><noRegion><name sortKey="Sutherland, Kate D" sort="Sutherland, Kate D" uniqKey="Sutherland K" first="Kate D" last="Sutherland">Kate D. Sutherland</name></noRegion><name sortKey="Alexander, Warren S" sort="Alexander, Warren S" uniqKey="Alexander W" first="Warren S" last="Alexander">Warren S. Alexander</name><name sortKey="Forrest, Natasha C" sort="Forrest, Natasha C" uniqKey="Forrest N" first="Natasha C" last="Forrest">Natasha C. Forrest</name><name sortKey="Holroyd, Sheridan L" sort="Holroyd, Sheridan L" uniqKey="Holroyd S" first="Sheridan L" last="Holroyd">Sheridan L. Holroyd</name><name sortKey="Lindeman, Geoffrey J" sort="Lindeman, Geoffrey J" uniqKey="Lindeman G" first="Geoffrey J" last="Lindeman">Geoffrey J. Lindeman</name><name sortKey="Mcmanus, Edward J" sort="Mcmanus, Edward J" uniqKey="Mcmanus E" first="Edward J" last="Mcmanus">Edward J. Mcmanus</name><name sortKey="Sutherland, Kate D" sort="Sutherland, Kate D" uniqKey="Sutherland K" first="Kate D" last="Sutherland">Kate D. Sutherland</name><name sortKey="Vaillant, Francois" sort="Vaillant, Francois" uniqKey="Vaillant F" first="François" last="Vaillant">François Vaillant</name><name sortKey="Visvader, Jane E" sort="Visvader, Jane E" uniqKey="Visvader J" first="Jane E" last="Visvader">Jane E. Visvader</name></country><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Wintermantel, Tim M" sort="Wintermantel, Tim M" uniqKey="Wintermantel T" first="Tim M" last="Wintermantel">Tim M. Wintermantel</name></region><name sortKey="Schutz, Gunther" sort="Schutz, Gunther" uniqKey="Schutz G" first="Gunther" last="Schutz">Gunther Schutz</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Watson, Christine J" sort="Watson, Christine J" uniqKey="Watson C" first="Christine J" last="Watson">Christine J. Watson</name></region></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Chodosh, Lewis A" sort="Chodosh, Lewis A" uniqKey="Chodosh L" first="Lewis A" last="Chodosh">Lewis A. Chodosh</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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