Jun-Lin Guan, Ph.D.
Professor
Dept of Internal Medicine-Division of
Molecular Medicine and Genetics
Dept of Cell and Developmental Biology
109 Zina Pitcher, Room 4013 BSRB
University of Michigan Medical School
Ann Arbor, MI 48109-2200
Tel: 734-615-4936
Fax: 734-615-2506
E-mail: jlguan@umich.edu

Go to Jun-Lin Guan's Lab Website

Research Focus:

Signal transduction in development and cancer

The goals of our research programs are to understand fundamental principles of cell signaling in the regulation of basic cellular functions in normal cell and developmental processes and to determine how disruption of the normal signaling pathways either by genetic mutations or environmental insults may lead to diseases such as cancer. One area of current interests is identification of signaling molecules and pathways involved in the regulation of cell migration and invasion as well as examination of the signaling networks involving cross-talks among different pathways. A second area of research focuses on the role of focal adhesion kinase (FAK), a cytoplasmic tyrosine kinase important in mediating signaling by integrins as well as some growth factor receptors, in the regulation of angiogenesis and cancer metastasis in vivo using mouse genetic approaches. Lastly, our lab has recently identified a protein inhibitor for FAK, FIP200, which has been shown to regulate a number of signaling pathways and is implicated as a putative tumor suppressor for breast cancer. We are using a combination of cell and molecular biological and mouse genetic approaches to clarify the potential role and mechanisms of FIP200 in development and cancer.

Relevant Publications:

1. Residues within the first subdomain of FAK’s FERM-like domain are important for its regulation. (2005). L.A. Cohen and J.-L. Guan. J. Biol. Chem. 280: 8197-8207.



2. Conditional knockout of focal adhesion kinase in endothelial cells reveals its role in angiogenesis and vascular development in late embryogenesis. (2005). T.-L. Shen, A. Park, A. Alcaraz, X. Peng, I. Jang, P. Koni, R. Flavell, H. Gu and J.-L. Guan. J. Cell Biol. 169: 941-952.



3. The mechanisms of the cell cycle arrest by FIP200 in human breast cancer cells. (2005). Z. Melkoumian, X. Peng, B. Gan, X. Wu and J.-L. Guan. Cancer Research. 65, 6676-6684.



4. Identification of FIP200 interaction with TSC1-TSC2 complex and its role in regulation of cell size control. (2005). B. Gan, Z. Melkoumian, X. Wu, K.-L. Guan, and J.-L. Guan. J. Cell Biol. 170, 379-389.



5. FAK-mediated Src phosphorylation of Endophilin A2 inhibits endocytosis of MT1-MMP and promotes ECM degradation. (2005). X. Wu, B. Gan, Y. Yoo and J.-L. Guan. Dev. Cell. 9, 185-196. (Featured article in this issue).



6. Inactivation of FAK in cardiomyocytes promotes cardiac eccentric hypertrophy and fibrosis in mice. (2006). X. Peng, M. S. Kraus, H. Wei, T.-L. Shen, R. Pariaut, A. Alcaraz, G. Ji, L. Cheng, Q. Yang, M. I. Kotlikoff, J. Chen, K. Chien, H. Gu and J.-L. Guan. J. Clin. Invest. 116: 217-227.



7. Regulation of RNA polymerase II-dependent transcription by N-WASP and its nuclear binding partners. (2006). X. Wu, Y.Yoo, N. N. Okuhama, P. W. Tucker, G. Liu and J.-L. Guan. Nat. Cell Biol. 8: 756-763. (Also see NCB News and Views p650-651 in the same issue; and Leading Edge: Cell 126, 431-433, 2006).



8. Role of FIP200 in cardiac and liver development and its regulation of TSC-mTOR and TNFa signaling pathways. (2006). B. Gan, X. Peng, T. Nagy, A. Alcaraz, H. Gu and J.-L. Guan. J. Cell Biol. 175: 121-133.