| First Author | Kim H | Year | 2005 |
| Journal | Oncogene | Volume | 24 |
| Issue | 36 | Pages | 5629-36 |
| PubMed ID | 16007215 | Mgi Jnum | J:100783 |
| Mgi Id | MGI:3589531 | Doi | 10.1038/sj.onc.1208718 |
| Citation | Kim H, et al. (2005) c-Src-null mice exhibit defects in normal mammary gland development and ERalpha signaling. Oncogene 24(36):5629-36 |
| abstractText | The c-Src tyrosine kinase has been implicated to play an integral role in modulating growth factor receptor, integrin and steroid receptor function. One class of steroid receptors that c-Src modulates is the estrogen receptor alpha (ERalpha). Although there is strong biochemical evidence supporting a role for c-Src in ERalpha signaling, the consequence of this association is unclear at the biological level. To explore the significance of c-Src in ERalpha signaling, we studied the development of various reproductive organs that are dependent on ERalpha in c-Src-deficient mice. We show that the loss of the c-Src tyrosine kinase correlates with defects in ductal development as well as in uterine and ovarian development. Genetic and biochemical analyses of c-Src-deficient mammary epithelial cells also revealed defects in the ability of mammary epithelial cells to activate a number of signaling pathways in response to exogenous estrogen stimulation. Taken together, these studies demonstrate that c-Src plays a role in ERalpha signaling in vivo. |
