PUBLICATIONS DESCRIBING OUR THIAMINE RESEARCH
Martin, P.R., McCool, B.A., and Singleton, C.K. (1993). Genetic sensitivity
to thiamine deficiency and development of alcoholic organic brain disease.
Alcoholism: Clin. and Exp. Res. 17, 31-37.
McCool, B., Plonk, S., Martin, P.R., and Singleton, C.K. (1993). Cloning
of human transketolase cDNAs and comparison of the nucleotide sequence of
the coding region in Wernike-Korsakoff and non-Wernicke-Korsakoff individuals.
J. Biol. Chem. 268,1397-1404.
Martin, P. R., Pekovich, S. R., McCool, B. A., Whetsell, W. O., and Singleton,
C. K. (1994). Thiamine utilization in the pathogenesis of alcohol-induced
brain damage. Alcohol Alcohol. 2S, 273-279.
Singleton, C.K., Pekovich, S.R., McCool, B.A., and Martin, P.R. (1995).
Hysteretic behavior of human transketolase: implications for thiamine deficiency.
J. Nutrition 125, 189-194.
Martin, P. R., McCool, B. A., and Singleton, C. K. (1995). Molecular Genetics
of transketolase and its role in the pathogenesis of the Wernicke-Korsakoff
syndrome. Metab. Brain Disease 10, 45-55.
Pekovich, S. R., Martin, P. R., and Singleton, C. K. (1996). Thiamine pyrophosphate-requiring
enzymes are altered during pyrithiamine-induced thiamine deficiency in cultured
human lymphoblasts. J. Nutrition 126, 1791-1798.
*Singleton, C. K., Wang, J. J.-L., Shan, L., and Martin, P. R. (1996). Conserved
residues are functionally distinct within transketolases from different
species. Biochemistry 35, 15865-15869.
*Wang, J. J.-L., Martin, P. R. and Singleton, C. K. (1997). Transketolase
assembly defect in a Wernicke-Korsakoff Syndrome patient. Alc. Clin. Exp.
Res. 21, 576-580. PDF
*Wang, J.-L., Martin, P. R., and Singleton, C. K. (1997). Aspartate 155
of human transketolase is essential for thiamine pyrophosphate-magnesium
binding, and cofactor binding is required for dimer formation. Biochem.
et. Biophys. Acta 1341, 165-172. PDF
*Singleton, C. K. (1997). Identification and characterization of the thiamine
transporter gene of Saccharomyces cereviciae. Gene 199, 111-121. PDF
*Pekovich, S. R., Martin, P. R., Poggi, V. and Singleton, C. K. (1998).
Sensitivity to thiamine deficiency in cultered human cells is dependent
on cell type and is enhanced in cells from thiamine-responsive megaloblastic
anemia patients. J. Nutri. Biochem. 9, 215-222. PDF
*Pekovich, S. T., Martin, P.R., and Singleton, C. K. (1998). Thiamine deficiency
decreases the steady-state mRNA levels for transketolase and pyruvate dehydrogenase
but not for a-ketoglutarate dehydrogenase in three human cell types. J.
Nutr. 128, 683-687. PDF
Ragan, P. W., Singleton, C. K., and Martin, P. R. (1999). Brain injury associated
with chronic alcoholism. CNS Spectrums 4, 66-87.
*Wang, J. J-L., Fentress, H., Hua, Z. and Singleton, C. K. JNK1 is inactivated
during thiamine deficiency-induced apoptosis in human neruoblastoma cells.
J. Nutri. Biochem. 11, 208-215. PDF
*Singleton, C. K., (2001). Transketolase. in Encyclopedia of Molecular
Medicine, Thomas E. Creighton, editor. 3224-3226.
**Singleton, C.K. and Martin, P. R. (2001). Molecular effects of thiamine
deficiency. Cur. Mol. Med. 1, 197-208. PDF
**Song, T. and Singleton, C.K. (2002). Mitochondria from cultured cells
derived from normal and thiamine-responsive megaloblastic anemia individuals
efficiently import thiamine diphosphate. BMC Biochemistry 3, 8 PDF
Peter R. Martin, Charles K. Singleton, and Susanne Hiller-Sturmhfel. (2004).
The Role of Thiamine Deficiency in Alcoholic Brain Disease. Alcohol Research
& Health 27, 134-142. PDF