| First Author | Lindeman GJ | Year | 2001 |
| Journal | Genes Dev | Volume | 15 |
| Issue | 13 | Pages | 1631-6 |
| PubMed ID | 11445538 | Mgi Jnum | J:70408 |
| Mgi Id | MGI:2137168 | Doi | 10.1101/gad.880801 |
| Citation | Lindeman GJ, et al. (2001) SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice. Genes Dev 15(13):1631-6 |
| abstractText | 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. |
