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Publication : Lactation defect in mice lacking the helix-loop-helix inhibitor Id2.

First Author  Mori S Year  2000
Journal  EMBO J Volume  19
Issue  21 Pages  5772-81
PubMed ID  11060028 Mgi Jnum  J:65670
Mgi Id  MGI:1927032 Doi  10.1093/emboj/19.21.5772
Citation  Mori S, et al. (2000) Lactation defect in mice lacking the helix-loop-helix inhibitor Id2. EMBO J 19(21):5772-81
abstractText  Id proteins are thought to be negative regulators of cell differentiation and positive regulators of cell proliferation. Mammary glands of Id2(-/-) female mice reveal severely impaired lobulo-alveolar development during pregnancy. Id2(-/-) mammary epithelia show no precocious maturation, but instead exhibit intrinsic defects in both cell proliferation and cell survival, implying that the role of Id2 in pregnant mammary epithelia is mainly stimulation of cell proliferation and support of cell viability. Expression studies of genes required for mammary gland development suggest Id2 to be a downstream or parallel factor of these genes. A decrease in the DNA binding activity of Stat5 was also observed in Id2(-/-) mammary glands at 7 days post-coitus. Our results indicate an indispensable role of Id2 in pregnant mammary glands.
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