Research Publications

Back

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


Lindeman, GJ; Wittlin, S; Lada, H; Naylor, MJ; Santamaria, M; Zhang, JG; Starr, R; Hilton, DJ; Alexander, WS; Ormandy, CJ; Visvader, J
2001-07-01
GENES & DEVELOPMENT
Journal Article
15
13
1631-1636
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.
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
SIGNAL-TRANSDUCTION; LACKING SUPPRESSOR; CYTOKINE; PROTEIN; LIVER; ACTIVATION; INHIBITOR; PATHWAYS; BINDING; FAMILY
10.1101/gad.880801
Refer to copyright notice on published article.

Back
Creation Date 2001-07-01 12:00:00