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Microsomal arylacetamide deacetylase competes against the activity of cytosolic arylamine N-acetyltransferase, which catalyzes one of the initial biotransformation pathways for arylamine and heterocyclic amine carcinogens [provided by RefSeq, Jul 2008].. Additionally we are shipping Arylacetamide Deacetylase (Esterase) Proteins (10) and many more products for this protein.
Showing 10 out of 44 products:
Human Monoclonal AADAC Primary Antibody for ELISA, WB - ABIN513029
Watanabe, Fukami, Nakajima, Takamiya, Aoki, Yokoi: Human arylacetamide deacetylase is a principal enzyme in flutamide hydrolysis. in Drug metabolism and disposition: the biological fate of chemicals 2009
Show all 5 references for ABIN513029
Human Monoclonal AADAC Primary Antibody for ELISA, WB - ABIN393404
Rose, Behm, Drgon, Johnson, Uhl: Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. in Molecular medicine (Cambridge, Mass.) 2010
Show all 5 references for ABIN393404
Human Polyclonal AADAC Primary Antibody for FACS, IHC (p) - ABIN390780
Saito, Iida, Sekine, Kawauchi, Higuchi, Ogawa, Nakamura: Catalog of 680 variations among eight cytochrome p450 ( CYP) genes, nine esterase genes, and two other genes in the Japanese population. in Journal of human genetics 2003
Human Polyclonal AADAC Primary Antibody for WB - ABIN2782106
Frick, Atanasov, Arnold, Ozols, Odermatt: Appropriate function of 11beta-hydroxysteroid dehydrogenase type 1 in the endoplasmic reticulum lumen is dependent on its N-terminal region sharing similar topological determinants with 50-kDa esterase. in The Journal of biological chemistry 2004
Data suggest that AADAC in hepatocyte microsomes hydrolyzes ketoconazole, a synthetic imidazole antifungal agent, to N-deacetyl ketoconazole and thus triggers hepatocellular toxicity.
AADAC deletion is a candidate susceptibility factor for Gilles de la Tourette Syndrome
Translational N-glycosylation of AADAC plays a crucial role in regulating AADAC enzyme activity.
Lipolysis of cellular TG and VLDL production were impaired in HCV infected cells during the early peak of viral infection. This was partially explained by an apparent deficiency of a putative TG lipase (show LIPG Antibodies), arylacetamide deacetylase (AADAC).
An AADAC*3 allele yields decreased enzyme activity in liver microsomes.
human AADAC was the enzyme responsible for the deacetylation of rifamycins and would affect the induction rate of drug-metabolizing enzymes by rifamycins and their induced hepatotoxicity.
two intrinsic endoplasmic reticulum (ER) proteins, 11beta-hydroxysteroid dehydrogenase, isozyme 1 (11beta-HSD (show CHST3 Antibodies)) and the 50-kDa esterase (show ESD Antibodies) (E3), sharing some amino acid sequence motifs in their N-terminal transmembrane (TM) domains.
Expression of AADA cDNA in McArdle-RH7777 cells significantly reduced intracellular triacylglycerol levels and apolipoprotein B (show APOB Antibodies) secretion and increased fatty acid oxidation.
Microsomal arylacetamide deacetylase competes against the activity of cytosolic arylamine N-acetyltransferase, which catalyzes one of the initial biotransformation pathways for arylamine and heterocyclic amine carcinogens
arylacetamide deacetylase (esterase)
, arylacetamide deacetylase-like
, Arylacetamide deacetylase
, arylacetamide deacetylase
, arylacetamide deacetylase-like 2