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

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Duffy, S.L. et al.

Shannon L. Duffy, Mark G. Coulthard, Mark D. Spanevello, Nirmitha I. Herath, Trina M. Yeadon, Jennifer K. McCarron, Jacinta C. Carter, Ian D. Tonks, Graham F. Kay, Gael E. Phillips, Andrew W. Boyd,

Generation and characterization of EphA1 receptor tyrosine kinase reporter knockout mice.

Eph receptor tyrosine kinases (RTKs) are a highly conserved family of signaling proteins with functions in cellular migration, adhesion, apoptosis, and proliferation during both adult and embryonic life. Here, we describe a knock-in mouse in which EphA1 expression is disrupted via the insertion of an internal ribosome entry site (IRES)-human placental alkaline phosphatase (ALPP) reporter cassette into exon II of the EphA1 gene. This was shown to successfully knockout expression of endogenous EphA1 and enforce expression of the ALPP reporter by the EphA1 promoter. Staining for the ALPP reporter protein demonstrated an epithelially restricted expression pattern in mouse tissues. In EphA1 null mice, two separate phenotypes were identified: abnormal tail development manifesting as a kinky tail was found in approximately 80% of homozygous adults. A second, distinct abnormality present in approximately 18% of females was characterized by imperforate uterovaginal development with hydrometrocolpos and caused by a resistance of cells to apoptosis during reproductive tract canalization. These results indicate a possible role for EphA1 in tissue patterning and hormone-induced apoptotic processes.[1]

References

Generation and characterization of EphA1 receptor tyrosine kinase reporter knockout mice. Duffy, S.L., Coulthard, M.G., Spanevello, M.D., Herath, N.I., Yeadon, T.M., McCarron, J.K., Carter, J.C., Tonks, I.D., Kay, G.F., Phillips, G.E., Boyd, A.W. Genesis (2008) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

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