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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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.[1]

References

  1. SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice. 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. Genes Dev. (2001) [Pubmed]
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