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Faculty Detail    
Name AIMEE LANDAR
Assistant Professor
 
Campus Address BMR2 506 Zip 2182
Phone 205-975-9507
E-mail landar@uab.edu
Other websites
     

Education
Undergraduate  University of South Alabama    1993  B.M. 
Graduate  University of South Alabama    1998  Ph.D. 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Assistant Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Assistant Professor
Center  Medicine  Comprehensive Diabetes Ctr Assistant Professor
Center  Medicine  Ctr Cardiovasc Bio Assistant Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Molecular and Cellular Pathology Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Aimee Landar, Ph.D. is an Assistant Professor at the University of Alabama at Birmingham. She received her Bachelor of Music degree in Flute Performance in 1993, and went on to earn a Ph.D. in Basic Medical Sciences-Pharmacology in 1998 from the University of South Alabama in Mobile, Alabama. Her postdoctoral training began in 1998 at the University of Alabama at Birmingham. She was promoted to Instructor in 2005, and to Research Assistant Professor from 2006-2009. She joined the tenure-earning faculty in 2009 as Assistant Professor.

Society Memberships
Organization Name Position Held Org Link
Society for Free Radical Biology and Medicine  Council Member   

Research/Clinical Interest
Title
Cell signaling by electrophiles
Description
The major area of interest of my research program is redox cell signaling, especially by electrophilic compounds. Electrophiles modify specific residues of proteins, (e.g. low pKa cysteine residues), and affect cellular processes such as migration, antioxidant responses, resolution of inflammation, and mitochondrial metabolism. Electrophile-signaling plays an important role in normal physiology, but may also be useful in the development of novel pharmacological agents for inflammatory diseases and cancer. We have developed a novel series of mitochondria-targeted soft electrophiles (MTSEs) which we are testing in cell and preclinical models of cancers with abnormally high levels of mitochondrial metabolism. MTSEs accumulate within the mitochondrion and post-translationally modify specific cysteine residues of metabolic proteins. We have also shown that MTSEs alter metabolic pathways and stop cancer cell growth. We are exploring the mechanisms by which MTSEs mediate cellular responses by using metabolomics and proteomics, in combination with candidate protein approaches. We hope to develop these and other electrophilic compounds to help treat and prevent human pathologies, such as cancer.

Selected Publications 
Publication PUBMEDID
Diers, A.D.*, Vayalil, P.K.*, Oliva, C.R., Griguer, C.E., Dranka, B.P, Darley-Usmar, V.M., Hurst, D.R., Welch, D.R., Landar, A. Mitochondrial bioenergetics of metastatic breast cancer cells in response to dynamic changes in oxygen tension: Effects of HIF-1α. PLoS One 8(6):e68348, 2013. PMCID:PMC3696014  PMID:23840849 
Wall SB, Oh JY, Diers AR, Landar A. Oxidative modification of proteins: an emerging mechanism of cell signaling. Front Physiol. 3:369 2012 [Epub Sep 14,2012]   PMID:23049513 
Bodenstine, T.M., Vaidya, K.S., Ismail, A., Beck, B.H., Diers, A.R., Edmonds, M.D., Kirsammer, G.T., Landar, A., Welch, D.R. Subsets of ATP-sensitive potassium channel (KATP) inhibitors increase gap junctional intercellular communication in metastatic cancer cell lines independent of SUR expression. FEBS Lett. 586(1):27-31, 2012. PMCID: PMC3249498 [Available on 2013/1/2]  PMID:22119728 
Diers, A.R., Dranka, B.P., Ricart, K.C., Oh, J.Y., Johnson, M.S., Zhou, F., Pallero, M.A., Bodenstine, T., Murphy-Ullrich, J.E., Welch, D.R., Landar, A. Modulation of mammary cancer cell migration by 15-deoxy-Δ12,14-prostaglandin J2: implications for anti-metastatic therapy. Biochem. J. 430(1):69-78, 2010  PMID:20536428 
Diers, A.R., Higdon, A.N., Ricart, K.C., Johnson, M.S., Agarwal, A., Kalyanaraman, B., Landar, A., Darley-Usmar, V.M. Mitochondrial targeting of an electrophile increases apoptotic efficacy via redox cell signaling mechanisms. Biochem. J. 426(1):31-41, 2010.  PMID:19916962 
Ricart, K.C., Bolisetty, S., Johnson, M.S., Perez, J., Agarwal, A., Murphy, M.P., Landar, A. A permissive role of mitochondria in the induction of HO-1 in endothelial cells. Biochem J. 419(2):427-36, 2009.   PMID:19161347 
Oh, J.-Y., Giles, N.M., Landar, A., Darley-Usmar, V. Accumulation of 15-deoxy-delta 12,14-prostaglandin J2 adduct formation with Keap1 over time: effects on potency for intracellular antioxidant defense induction. Biochem J. 411 (2):297-306, 2008.   PMID:18237271 
Gutierrez, J., Ballinger, S.W., Darley-Usmar, V.M., Landar, A. Free radicals, mitochondria, and oxidized lipids: the emerging role in signal transduction in vascular cells. Circ Res. 99(9):924-32, 2006.   PMID:17068300 
Landar, A., Zmijewski, J.W., Dickinson, D.A., Le Goffe, C.L., Johnson, M.S., Milne, G.L., Zanoni, G., Vidari, G., Morrow, J.D., and Darley-Usmar, V.M. The interaction of electrophilic lipid oxidation products with mitochondria in endothelial cells and the formation of reactive oxygen species. Am. J. Physiol. Heart Circ. Physiol. 290(5):H1777-87, 2006.
 
PMID:16387790 
Landar, A., Shiva, S., Levonen, A-L., Oh, J-Y., Zaragoza, C., Johnson, M.S., Darley-Usmar, V.M. Induction of the Permeability Transition and Cytochrome c Release by 15-deoxy Prostaglandin J2 in Mitochondria. Biochem. J. 394(Pt 1):185-195, 2006.   PMID:16268779 

Keywords
cell signaling, redox, electrophile, cancer, oxidative stress, mitochondria, metabolism