Phang-Lang Chen
Biological Chemistry, School of Medicine
Phone: (949) 824-4008
Email: plchen@uci.edu
http://www.healthaffairs.uci.edu/biochem/faculty/chen.html
Phang-Lang Chen
Dr. Chen’s laboratory is interested in understanding the critical role of tumor suppressor genes in the genesis and progression of cancer. Currently, they are putting most of their efforts into elucidating the intracellular signaling pathways involved in the DNA damage response. They are focusing on molecules serving as transducers and effectors, including BRCA1 and BRCA2, members of the BRCT motif-containing family proteins such as NBS1, 53BP1 and NFBD1, and on the DNA repair machinery. Understanding these signal pathways is vital for solving the puzzle of how cells maintain their genome stability and how specific problems with DNA repair predispose to different cell type-specific cancers.
Selected Publications:
Shang, Y. L., Bodero, A. J., and Chen, P. L. (2003). NFBD1, a novel nuclear protein with signature motifs of FHA and BRCT, and an internal 41-amino acid repeat sequence, is an early participant in DNA damage response. J Biol Chem 278(8), 6323-9.
Peng, A., and Chen, P. L. (2003). NFBD1, like 53BP1, is an early and redundant transducer mediating Chk2 phosphorylation in response to DNA damage. J Biol Chem 278(11), 8873-6.
Chen, P. L., Liu, F., Cai, S., Lin, X., Li, A., Chen, Y., Gu, B., Lee, E. Y., and Lee, W. H. (2005). Inactivation of CtIP leads to early embryonic lethality mediated by G1 restraint and to tumorigenesis by haploid insufficiency. Mol Cell Biol 25(9), 3535-42.
Peng, A., and Chen, P. L. (2005). NFBD1/Mdc1 mediates ATR-dependent DNA damage response. Cancer Res 65(4), 1158-63.
Furuta, S., Wang, J. M., Wei, S., Jeng, Y. M., Jiang, X., Gu, B., Chen, P. L., Lee, E. Y., and Lee, W. H. (2006). Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads to accelerated mammary tumor growth contributed by prominent vasculature. Cancer Cell 10(1), 13-24. |
