SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice
Prolactin is essential for proliferation and differentiation of the developing mammary gland. We have explored a role for Suppressor of Cytokine Signaling 1 (SOCS1) as a modulator of the prolactin response using mice deficient in SOCS1, which were rescued from neonatal death by deletion of the Interferon gamma (IFN gamma) gene. SOCS1(-/-)/IFN gamma(-/-) mice exhibited accelerated lobuloalveolar development in the mammary gland during late pregnancy and precocious lactation. Significantly, the lactogenic defect in prolactin receptor heterozygous females could be rescued by deletion of a single SOCS1 allele. These findings establish a role for SOCS1 as a negative regulator of prolactin signaling and suggest that SOCS1 is required for the prevention of lactation prior to parturition.
|Authors||Lindeman, G. J.;Wittlin, S.;Lada, H.;Naylor, M. J.;Santamaria, M.;Zhang, J. G.;Starr, R.;Hilton, D. J.;Alexander, W. S.;Ormandy, C. J.;Visvader, J. :|
|Responsible Garvan Author|
|Publisher Name||Genes Dev|
|URL link to publisher's version||http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11445538|