Dr. Jonathan Shillingford
joined our laboratory in February of 1998 as a postdoctoral research fellow after completing his Ph.D. program at the Hannah Research Institute, Scotland and the University of Wales
, Aberystwyth where he worked on the identification and characterization of glucose and phoshpate membrane transport processes in the mammary gland. Since arriving in the lab, he has worked on a variety of projects in the area of signal transduction and membrane transport. Jonathan's primary research focus has been the investigation of the tyrosine kinase, Jak2, and its role in the development of the mammary gland and its contribution to breast cancer and is the recipient of a 3-year grant from the DoD Breast Cancer Research Program. His other research interests include the analysis of signal transduction pathways as they relate to mammary gland development, the molecular identification and function of membrane transport processes and their contribution to mammary epithelial cell development, and the identification of membranous protein markers as a tool to aid in the proteotyping of mammary-associated developmental lesions observed in transgenic and knockout mouse models.
In September of 2003 Jonathan moved to the Lerner Institute at the Cleveland Clinic in Cleveland, Ohio, to take a Research Associate position. In July of 2005 Jonathan migrated with the lab to the University of California, Santa Barbara, where he is now a Project Scientist working on the cellular mechanisms that contribute to the development of polycystic kidney disease (PKD).
1. Long, W., Wagner, K.U., Lloyd, K.C.K., Binart, N., Shillingford, J.M., Hennighausen, L. and Jones, F. (2003) Conditional deletion of Erbb4 in the mammary gland identifies ErbB4 as an obligate mediator of Stat5 activation and epithelial functional differentiation. Development, 130, 5257-5268.
2. Bierie, B., Nozawa, M., Renou, J.-P., Shillingford, J.M., Morgan, F., Oka, T., Taketo, M.M., Cardiff, R.D., Miyoshi, K., Wagner, K-U., Robinson, G.W. and Hennighausen, L. (2003). Activation of beta-catenin in prostate epithelium induces hyperplasias and squamous transdifferentiation. Oncogene 22:3875-3877
3. Shillingford, J.M., Miyoshi, K., Robinson, G.W., Bierie, B., Cao, Y., Karin, M. and Hennighausen, L.(2003). Proteotyping of mammary tissue from transgenic and gene knockout mice with immunohistochemical markers. A tool to define developmental lesions. J. Histochem. Cytochem. 51:555-565.
4. Shillingford, J.M., Miyoshi, K., Flagella, M., Shull, G.E. and Hennighausen, L. (2002). Mouse mammary epithelial cells express the Na-K-Cl cotransporter, NKCC1: characterization, localization, and involvement in ductal development and morphogenesis. Mol. Endocrinol. 16:1309-1321.
5. Shillingford, J.M., Miyoshi, K., Robinson, G.W., Grimm, S.L., Rosen, J.M., Neubauer, H., Pfeffer, K. and Hennighausen, L. (2002). Jak2 is an essential tyrosine kinase involved in pregnancy-mediated development of mammary secretory epithelium. Mol. Endocrinol. 16:563-570.
6. Miyoshi, K., Shillingford, J.M., Le Provost, F., Gounari, F., Bronson, R., von Boehmer, H., Taketo, M.M., Cardiff, R.D., Hennighausen, L. and Khazaie, K. (2002). Activation of beta-catenin signaling in differentiated mammary secretory cells induces transdifferentiation into epidermis and squamous metaplasias. Proc. Natl. Acad. Sci. 99:219-224.
7. Walton, K.D., Wagner, K.U., Rucker, E.B. 3rd, Shillingford, J.M., Miyoshi, K. and Hennighausen, L. (2001). Conditional deletion of the bcl-x gene from mouse mammary epithelium results in accelerated apoptosis during involution but does not compromise cell function during lactation. Mech. Dev. 109:281-293.
8. Miyoshi, K., Shillingford, J.M., Smith, G.H., Grimm, S.L., Wagner, K.U., Oka, T., Rosen, J.M., Robinson, G.W. and Hennighausen, L. (2001). Signal transducer and activator of transcription (Stat) 5 controls the proliferation and differentiation of mammary alveolar epithelium. J. Cell. Biol. 155:531-542.
9. Shillingford, J.M. and Hennighausen, L. (2001). Experimental mouse genetics -- answering fundamental questions about mammary gland biology. Trends Endocrinol. Metab. 12:402-408. Review.
10. Sun, Y., Boyd, K., Xu, W., Ma, J., Jackson, C.W., Fu, A., Shillingford, J.M., Robinson, G.W., Hennighausen, L., Hitzler, J.K., Ma, Z. and Morris, S.W.(2006). Acute myeloid leukemia-associated Mkl1 (Mrtf-a) is a key regulator of mammary gland function. Mol. Cell. Biol. 26:5809-5826.
11.Cases, S., Zhou, P., Shillingford, J.M., Wiseman, B.S., Fish, J.D., Angle, C.S., Hennighausen, L., Werb, Z. and Farese, Jr., R.V. (2004). Development of the mammary gland requires DGAT1 expression in stromal and epithelial tissues. Development. 131:3047-3055.