Influence of estrogens on mouse uterine epidermal growth factor precursor protein and messenger ribonucleic acid.
Investigating whether an epidermal growth factor (EGF)-related polypeptide originates in the uterus of the immature or adult mouse under normal or altered estrogen status suggests that EGF occurs predominantly as the membrane-bound precursor form in this organ, as has been previously shown for the kidney.
Requirement of Estrogen Receptor-α in Insulin-like Growth Factor-1 (IGF-1)-induced Uterine Responses and in Vivo Evidence for IGF-1/Estrogen Receptor Cross-talk*
Functional signaling proximal to IGF-1R is maintained in the αERKO mouse uterus, ERα is necessary for IGF- 1 induction of uterine nuclear proliferative responses, and cross-talk between IGF-2R and ER signaling pathways exists in vivo are demonstrated.
Physiological coupling of growth factor and steroid receptor signaling pathways: estrogen receptor knockout mice lack estrogen-like response to epidermal growth factor.
- S. Curtis, T. Washburn, K. Korach
- BiologyProceedings of the National Academy of Sciences…
- 29 October 1996
The coupling of EGF and ER signaling pathways in the rodent reproductive tract is demonstrated, conclusively demonstrating the requirement for ER in an in vivo system.
Expression and functional properties of transforming growth factor alpha and epidermal growth factor during mouse mammary gland ductal morphogenesis.
The results indicate that an EGF-receptor-mediated pathway remained intact in the mammary gland epithelium in the absence of ovarian steroids and that local availability of either EGF or TGF-alpha is sufficient to stimulate the pattern of normal ductal growth.
Myelination Is Altered in Insulin-Like Growth Factor-I Null Mutant Mice
- P. Ye, Liqin Li, R. Richards, R. Diaugustine, A. D'ercole
- Biology, ChemistryJournal of Neuroscience
- 15 July 2002
It is found that myelin staining, MBP and PLP expression, and the percentage of oligodendrocytes and their precursors are significantly reduced in all brain regions of developing IGF-I KO mice but are similar to controls in adult IGF-i KO mice, suggesting that IGF-II can compensate in part for IGF- I actions on myelination.
Expression of NAG-1, a Transforming Growth Factor-β Superfamily Member, by Troglitazone Requires the Early Growth Response Gene EGR-1*
- S. Baek, Jongsik Kim, J. Nixon, R. Diaugustine, T. Eling
- BiologyJournal of Biological Chemistry
- 20 February 2004
The results suggest that EGR-1 induction is a unique property ofTGZ, but is independent of PPARγ activation, and the up-regulation of NAG-1 may provide a novel explanation for the antitumorigenic property of TGZ.
Proliferation of mouse uterine epithelial cells in vitro.
A defined culture system for mouse uterine epithelial cells is established to aid in investigations on hormonal effects on the growth and differentiation of estrogen target cells and showed that the attachment and growth of these cells on collagen were markedly influenced by the calcium concentration.
Mammary gland branching morphogenesis is diminished in mice with a deficiency of insulin-like growth factor-I (IGF-I), but not in mice with a liver-specific deletion of IGF-I.
It is proposed that paracrine, not endocrine, IGF-I is important for mammary branching morphogenesis, and that GH is required for Mammary gland ductal morphogenesis.
Activation and function of the epidermal growth factor receptor and erbB-2 during mammary gland morphogenesis.
- J. Sebastian, R. Richards, R. Diaugustine
- BiologyCell growth & differentiation : the molecular…
- 1 September 1998
Examining extracts of inguinal mammary glands from prepubertal and pubertal mice for tyrosine-phosphorylated EGFR and other erbB receptors suggested that EGFR is essential for morphogenesis of the mammary ducts and functions during this period of mammary development as a heterodimer with ErbB-2 in the Mammary stroma.
Activation of a Uterine Insulin-Like Growth Factor I Signaling Pathway by Clinical and Environmental Estrogens: Requirement of Estrogen Receptor-α.
It is demonstrated that several chemicals shown previously to display estrogenic activities also mimic E2 by activating uterine IGF-I signaling, indicating that ERalpha is required for activation of uterines IGF-IR by these diverse chemicals.