Ph.D., Stanford University, 1971
University of California, Irvine
B235/B210 Medical Sciences I
Mail Code 4025
Irvine, CA 92697-1700
Phone: (949) 824-7042, 5259
FAX: (949) 824-8598
ejstanbr@uci.edu
UCI Faculty Profile
Dr. Stanbridge's research concerns the molecular genetics of human cancer. In addition to activated oncogenes, a family of genes (called tumor suppressor genes) critically involved in the control of malignancy has been identified. Dr. Stanbridge has provided functional evidence for the role of tumor suppressor genes in human cancer using somatic cell hybrid and monochromosome transfer techniques. His group has also engaged in cloning candidate tumor suppressor genes. One of the functions of such genes appears to be negative regulation of transcription of tumor-associated antigens. One such regulated gene has been identified as intestinal alkaline phosphatase (IAP). The molecular basis of negative regulation is being studied using this gene as an experimental model. An important question in the field of cancer molecular genetics is whether there are interactions between tumor suppressor genes and activated oncogenes. Ongoing studies in the laboratory addressing this question involve homologous recombination experiments that disrupt gene function.
Another research interest of Dr. Stanbridge's is to develop molecular probes for the identification of microorganisms in clinical settings. Dr. Stanbridge was one of the early developers of the use of cloned fragments of ribosomal RNA genes as molecular probes for detection of mycoplasmas and other microorganisms in idiopathic diseases such as rheumatoid arthritis where an infectious etiology is suspected.
UCI Faculty Profile: Eric J. Stanbridge.
Kost-Alimova, M., Darai-Ramqvist,E., Yau, W.L., Sandlund, A., Federova,
L., Yang, Y., Kholodnyuk, I., Cheng, Y., Lung, M., Stanbridge, E.J.,
Klein, G., and Imreh, S. 2007. Mandatory chromosomal segment balance in
aneuploid cells. BMC Central (in press)
Wang, X.Q., Redpath,J.L., Fan, S.T., and Stanbridge, E.J. 2006. ATR
dependent activation of Chk2. J.Cell Physiol. 208: 613-619.
Kaluz, S., Kaluzova, M., and Stanbridge, E.J. 2006. Proteasomal inhibition
attenuates transcriptional activity of hypoxia-inducible factor1 (HIF-1)
via specific effect on the HIF-1? C-terminal activation domain. Mol. Cell.
Biol. 26: 5895-5907.
Kaluz, S., Kaluzova, M., and Stanbridge, E.J., 2006. The role of
extracellular signal-regulated protein kinase in transcriptional
regulation of the hypoxia marker carbonic anhydrase IX. J. Cell. Biochem.
97: 207-216.
Wang, ÊX.Q., Luk, ÊJ.M., Leung, ÊP.P., Wong, ÊB.W., Stanbridge, E.J., Êand
Fan, ÊS.T. 2005. Alternative mRNA splicing of liverintestine-cadherin in
hepatocellular carcinoma. Clin. Cancer Res. 11:483-489
Ivanova, A.V. Liao, S.Y., Lerman, M.I., Ivanov, S.V., and Stanbridge, E.J.
2005. STRA13 expression and subcellular localization in normal and tumor
tissues: implications for use as a diagnostic and differentiation marker.
J. Med. Genet. 42: 565-576.
Soughayer, J.S., Y. Wang, H. Li, S.-H. Cheung, F.M. Rossi, E.J. Stanbridge,
C.E. Sims, and N.L. Allbritton. 2004. Characterization of TAT-mediated
transport of detachable kinase substrates. Biochemistry
240:518-525.
Kaluzova, M., S. Kaluz, M.I. Lerman, and E.J. Stanbridge. 2004. DNA damage
is a prerequisite for p53-mediated proteasomal degradation of HIF-1? in
hypoxic cells and downregulation of the hypoxia marker carbonic anhydrase
IX. Mol. Cell Biol. 24:5757-5766.
List of Publications via PubMed (NIH National Library of Medicine)