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| Item Type: | Article |
|---|---|
| Title: | Negative regulation of Ros receptor tyrosine kinase signaling: An epithelial function of the SH2 domain protein tyrosine phosphatase SHP-1 |
| Creators Name: | Keilhack, H., Mueller, M., Boehmer, S.A., Frank, C., Weidner, K.M., Birchmeier, W., Ligensa, T., Berndt, A., Kosmehl, H., Gunther, B., Mueller, T., Birchmeier, C. and Boehmer, F.D. |
| Abstract: | Male "viable motheaten" (me(v)) mice, with a naturally occurring mutation in the gene of the SH2 domain protein tyrosine phosphatase SHP-1, are sterile. Known defects in sperm maturation in these mice correlate with an impaired differentiation of the epididymis, which has similarities to the phenotype of mice with a targeted inactivation of the Ros receptor tyrosine kinase. Ros and SHP-1 are coexpressed in epididymal epithelium, and elevated phosphorylation of Ros in the epididymis of me(v) mice suggests that Ros signaling is under control of SHP-1 in vivo. Phosphorylated Ros strongly and directly associates with SHP-1 in yeast two-hybrid, glutathione S-transferase pull-down, and coimmunoprecipitation experiments. Strong binding of SHP-1 to Ros is selective compared to six other receptor tyrosine kinases. The interaction is mediated by the SHP-1 NH(2)-terminal SH2 domain and Ros phosphotyrosine 2267. Overexpression of SHP-1 results in Ros dephosphorylation and effectively downregulates Ros-dependent proliferation and transformation. We propose that SHP-1 is an important downstream regulator of Ros signaling. |
| Keywords: | Protein Tyrosine Phosphatase, Regulation, Receptor Tyrosine Kinase, Epididymis, Fertility, Animals, Mice |
| Source: | Journal of Cell Biology |
| ISSN: | 0021-9525 |
| Publisher: | Rockefeller University Press |
| Volume: | 152 |
| Number: | 2 |
| Page Range: | 325-334 |
| Date: | 22 January 2001 |
| Additional Information: | Copyright (c) 2001 by The Rockefeller University Press |
| Official Publication: | https://doi.org/10.1083/jcb.152.2.325 |
| PubMed: | View item in PubMed |
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