ehong at lanl dot gov
B Div Communications
Host Pathogen Interactions
Dr. Hong-Geller graduated from Columbia University, NY with a BA in biochemistry in 1991. She obtained her Ph.D in Cell and Molecular Biology at MIT, MA in 1997 studying the quality control mechanisms in the secretory pathway that recognizes misfolded versus correctly-folded proteins in the lab of Dr. Chris Kaiser. She then was funded as an American Cancer Society Post-doctoral Fellow at Cornell University from 1997-2000 in the lab of Dr. Rick Cerione to study the role of small GTPases in the allergic response in mast cells. In 2000, she came to Biosciences Division at LANL as a post-doctoral associate with the Host-Pathogen Interactions Group and was converted to Technical Staff Member in 2003. She has worked on multiple host-pathogen projects at LANL, including design of molecular decoy molecules to combat S. aureus superantigen infection, host response to beryllium exposure, and regulation of Toll-like receptor 4 activity in the innate immune system. She has ~12 years experience working with molecular and cellular biology, mammalian cell culture and accompanying cellular assays in a host immune response system. Currently she is a PI on a LANL Laboratory Directed Research and Development Exploratory Research project (LDRD-ER) and a DTRA funded project which focus on the use of RNA interference technology to identify host genes targeted by pathogens during infection. In addition, she is a co-I on a LDRD Directed Research (LDRD-DR) project "Genomes to behavior: predicting bacterial response by constrained network interpolation", which uses Burkholderia spp. as a model system for developing regulatory gene networks that can be used to predict bacterial response in response to cellular stimuli. She is also funded by DHS to study bioforensics analysis of pathogens in the environment.
Hong-Geller, E., Valdez, Y., Shou, Y., Yoshida, T., Marrone, B., and Dunbar, J. (2009) Comparison of sample collection methods for virulent and non-virulent B. anthracis and Y. pestis. Submitted.
Hong-Geller, E. (2009) A role for cell adhesion in beryllium-mediated lung disease. In Journal of Occupational and Environmental Hygiene, In Press.
Lauer, S., Kunde, YA, Apodaca, TA, Goldstein, B., and Hong-Geller, E. (2009) Soluble MD2 increases TLR4 levels on the epithelial cell surface. Cell. Immunol. 255: 8-16.
Rodriguez, S., Kunde, YA, McClesky, TM, and Hong-Geller, E. (2008) Upregulation of I-CAM1 in response to beryllium exposure in small airway epithelial cells. Toxicol. Lett. 179: 140-7.
Hong-Geller, E, Chaudhary, A. and Lauer, S. (2008) Targeting Toll-like receptor signaling pathways for design of novel immune therapeutics. Current Drug Discovery Technologies. 5: 29-38.
Scott, BL., McCleskey, TM, Chaudhary, A., Hong-Geller, E, and Gnanakaran, S. (2008) The bioinorganic chemistry and associated immunology of chronic beryllium disease. Chem. Commun. 25: 2837-47.
Hong-Geller, E and Chaudhary, A. (2007) Chemokine function in granulomatous lung disease In Progress in Chemokine Research, W. P. Linkes ed. Nova Publishers.
Hong-Geller, E., Pardington, P., Cary, R., Sauer, N., and Gupta, G. 2006. Chemokine regulation in response to beryllium exposure in human peripheral blood mononuclear and dendritic cells. Toxiciology. 218:216-28.
Hong-Geller, E., Molhoff, M. Shiflett, P.R., and Gupta, G. 2004. Design of chimeric receptor mimics with different TcRV_ isoforms: type-specific inhibition of superantigen pathogenesis. J. Biol. Chem. 279:5676-5684.
Hong-Geller, E. and G. Gupta. 2003. Therapeutic approaches to superantigen-based diseases. J. Molec. Recog. 16:91-101.
Zhong, B., K. Jiang, D.L. Gilvary, P.K. Epling-Burnette, C. Ritchey, J. Liu, R.J. Jackson, E. Hong-Geller, and S. Wei. 2003. Human neutrophils utilize a Rac/Cdc42-dependent MAPK pathway to direct intracellular granule mobilization towards ingested microbial pathogens. Blood. 101:3240-3248.
Jiang, K., B. Zhong, B. Ritchey, D.L. Gilvary, E. Hong-Geller, S. Wei, and J.Y. Djeu. 2003. Regulation of AKT dependent cell survival by Syk and Rac. Blood. 101:236-44.
Jiang, K., Zhong, B., Gilvary, D.L., Corliss, B.C., Vivier, E., Hong-Geller, E., Wei, S. and J.Y. Djeu. 2002. Syk regulation of phosphoinositide 3-kinase-dependent NK cell function. J. Immun. 168:3155-64.
Hong-Geller, E., D.A. Holowka, R.P. Siraganian, B.A. Baird, and R.A. Cerione. 2001. Activation of PLC_1 by Cdc42/Rac during mast cell degranulation. Proc. Natl Acad Sci. 98:1154-1159.
Hong-Geller, E., K. Field, J. Apgar, R.P. Siraganian, B.A. Baird, and D.A. Holowka. 2000. Mutant RBL mast cells defective in Fc_R1 signaling and lipid raft biosynthesis are reconstituted by activated Rho-family GTPases. Mol. Biol. Cell. 11:3661-3673.
Hong-Geller, E., and R. Cerione. 2000. Cdc42 and Rac stimulate exocytosis of secretory vesicles by activating the IP3/calcium pathway in RBL-2H3 mast cells. J.Cell Biol. 148: 481-494.
Jiang, K., B. Zhong, D.L. Gilvary, B.C. Corliss, E. Hong-Geller, S. Wei, and J.Y. Djeu. 2000. Pivotal role of phosphoinositide-3 kinase in regulation of cytotoxicity in natural killer cells. Nature Immun. 1:419-425.
Hong, E., A.R. Davidson, and C.A. Kaiser. 1996. A pathway for targeting soluble misfolded proteins to the yeast vacuole. J.Cell Biol. 135:623-633.Patent: #20050260222 Structure-based receptor mimics targeted against bacterial superantigen toxins, Goutam Gupta, Elizabeth Hong-Geller, Patrick Shiflett, and Nancy Lehnert