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SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice

Abstract

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.

Type Journal
ISBN 0890-9369 (Print)
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. :
Garvan Authors Prof Chris Ormandy
Publisher Name Genes Dev
Published Date 2001-01-01 00:00:00
Published Volume 15
Published Issue 13
Published Pages 1631-6
URL http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11445538
Status Published In-print