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Molecules and Cells|May 8, 1998
The "VH1-like" dual-specificity protein tyrosine phosphatasesK J Martell, T Angelotti, A UllrichProceedings of the National Academy of Sciences of the United States of America|July 15, 1991
Diverse point mutations in the human gene for polymorphic N-acetyltransferaseK P Vatsis, K J Martell, W W WeberMolecular Pharmacology|August 1, 1992
Cloned mouse N-acetyltransferases: enzymatic properties of expressed Nat-1 and Nat-2 gene productsK J Martell, G N Levy, W W WeberPharmacogenetics|April 1, 1993
Polymorphic N-acetylation of 2-aminofluorene by cell-free colon extracts from inbred miceG N Levy, K J Martell, W W WeberPrincess Takamatsu Symposia|January 1, 1990
Polymorphic acetylation of arylamines and DNA-adduct formationW W Weber, G N Levy, K J MartellMolecular Pharmacology|August 1, 1991
Molecular genetic basis of rapid and slow acetylation in miceK J Martell, K P Vatsis, W W WeberThe Journal of Biological Chemistry|March 25, 1990
Elimination and reconstitution of the requirement for hormone in promoting temperature-dependent transformation of cytosolic glucocorticoid receptors to the DNA-binding stateS Meshinchi, E R Sanchez, K J Martell, et al.Pharmacogenetics|October 1, 1992
Metabolic, molecular genetic and toxicological aspects of the acetylation polymorphism in inbred miceG N Levy, K J Martell, J H DeLeon, et al.The Journal of Biological Chemistry|February 4, 1994
Isolation and characterization of a human dual specificity protein-tyrosine phosphatase geneS P Kwak, D J Hakes, K J Martell, et al.Drug Metabolism and Disposition: the Biological Fate of Chemicals|December 1, 1995
Slow acetylation in mice is caused by a labile and catalytically impaired mutant N-acetyltransferase (NAT2 9)J H De Leon, K J Martell, K P Vatsis, et al.Pageof 2