David S. McNabb, Ph.D.
 Associate Professor
University of Arkansas
Department of Biological Sciences SCEN601
Fayetteville, AR  72701
phone:  (479) 575-3797   FAX:  (479) 575-4010
email:   dmcnabb@uark.edu
Office:  SCEN526
Laboratory:  Ferritor Hall Rm. 317-320

Ph.D., LSU Medical School, Shreveport, LA, 1992.
Postdoctoral Fellow, Massachusetts Institute of Technology


Candida albicans engulfment by murine macrophage (photo by Erika Kroger).


Candida albicans escape from murine macrophages (photo by Erika Kroger).


Research projects:
Regulation of gene expression in Candida albicans and its relationship to pathogenesis
Role of respiratory metabolism in Candida albicans dimorphism and pathogenesis
Regulation of eukaryotic gene expression, protein-DNA interactions
Novel technologies for molecular genetics studies in eukaryote
DNA and protein analysis using nanopore technology (with Jiali Li, Dept. Physics)

Useful links:
Laboratory Protocols
Laboratory Members
Courses Taught by David
Useful Websites
Laboratory meetings
David's CV
To request strains/plasmids from the McNabb lab
Research funding
Lab research facilities

RESEARCH SUMMARY: The major focus of my research is understand the molecular mechanisms by which Candida albicans causes infection in humans. C. albicans is the most frequently encountered fungal pathogen in humans, and is responsible for both mucocutaneous and systemic infections. The incidence of Candida infections has been rising in recent years primarily in immunocompromised individuals. At the same time, the rise in drug resistance, as well as the inherent toxicities of certain antifungal therapies, makes it imperative to search for novel treatment approaches. Our goal is to evaluate whether the CCAAT-binding factor in C. albicans may serve as an antifungal drug target. The CCAAT-binding factor is a heterooligomeric transcriptional activator. Our current studies are focused on three main objectives: 1) to generate mutants in the genes encoding the various subunits of the CCAAT-binding factor and evaluate their phenotypes; 2) to determine whether the CCAAT-binding factor is important in C. albicans virulence using the mouse model; and 3) to dissect the regulatory function of the CCAAT-binding factor using standard molecular techniques.

SELECTED PUBLICATIONS:
McNabb, D.S., R.M. Reed, and R.A. Marciniak. 2005. A dual luciferase assay system for the rapid assessment of gene expression in Saccharomyces cerevisiae. Eukaryotic Cell 4:1539-1549.

Fologea, D., J. Uplinger, B. Thomas, D.S. McNabb, and J. Li. 2005. Slowing DNA translocation in a solid state nanopore. Nanoletters 5:1734-1737.

Johnson, D.C., K.E. Cano, E.C. Kroger, and D.S. McNabb. 2005. Identification of a novel function for the CCAAT-binding factor in Candida albicans. Eukaryotic Cell 4:1662-1676.

Fologea, D., M. Gershow, B. Ledden, D.S. McNabb, J.A.Golovchenko, and J. Li. 2005. Detecting pH denatured DNA with a solid state nanopore. Nanoletters 5:1905-1909.

McNabb, D.S. and I. Pinto. 2005. Assembly of the Hap2p/Hap3p/Hap4p/Hap5p-DNA complex in Saccharomyces cerevisiae. Eukaryotic Cell 4:1829-1839.

Fologea, D., B. Ledden, D.S. McNabb, and J. Li. 2007. Electrical characterization of protein molecules in a solid-state nanopore. Applied Physics Letters 91:053901.

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