Loss of function polymorphisms in NAT1 protect against spina bifida

[1]  L. E. Mitchell,et al.  The NAT1 C1095A polymorphism, maternal multivitamin use and smoking, and the risk of spina bifida. , 2005, Birth defects research. Clinical and molecular teratology.

[2]  Hui Li Goh,et al.  Genomic organization of human arylamine N-acetyltransferase Type I reveals alternative promoters that generate different 5'-UTR splice variants with altered translational activities. , 2005, The Biochemical journal.

[3]  J. Dairou,et al.  Inactivation of human arylamine N-acetyltransferase 1 by hydrogen peroxide and peroxynitrite. , 2005, Methods in enzymology.

[4]  R. Rozmahel,et al.  Generation and functional characterization of arylamine N-acetyltransferase Nat1/Nat2 double-knockout mice. , 2003, Molecular pharmacology.

[5]  D. Hein Molecular genetics and function of NAT1 and NAT2: role in aromatic amine metabolism and carcinogenesis. , 2002, Mutation research.

[6]  R. Berry,et al.  Folic acid alone prevents neural tube defects: evidence from the China study. , 2002, Epidemiology.

[7]  J. Adjaye,et al.  Expression of arylamine N-acetyltransferases in pre-term placentas and in human pre-implantation embryos. , 2000, Human molecular genetics.

[8]  M. Doll,et al.  Molecular genetics and epidemiology of the NAT1 and NAT2 acetylation polymorphisms. , 2000, Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology.

[9]  E. Sim,et al.  A method for genotyping murine arylamine N-acetyltransferase type 2 (NAT2): a gene expressed in preimplantation embryonic stem cells encoding an enzyme acetylating the folate catabolite p-aminobenzoylglutamate. , 1999, Biochemical pharmacology.

[10]  B. Futscher,et al.  Developmental expression of N-acetyltransferases in C57BI/6 mice. , 1999, Drug metabolism and disposition: the biological fate of chemicals.

[11]  V. Perry,et al.  Immunochemical detection of arylamine N-acetyltransferase during mouse embryonic development and in adult mouse brain. , 1998, Teratology.

[12]  R. T. Lie,et al.  Distinguishing the effects of maternal and offspring genes through studies of "case-parent triads". , 1998, American journal of epidemiology.

[13]  C R Weinberg,et al.  A log-linear approach to case-parent-triad data: assessing effects of disease genes that act either directly or through maternal effects and that may be subject to parental imprinting. , 1998, American journal of human genetics.

[14]  M. Levene,et al.  Prevention of neural-tube defects , 1993, The Lancet.

[15]  E. Sim,et al.  Purification of recombinant human N-acetyltransferase type 1 (NAT1) expressed in E. coli and characterization of its potential role in folate metabolism. , 1995, Biochemical pharmacology.

[16]  R. Minchin Acetylation of p-aminobenzoylglutamate, a folic acid catabolite, by recombinant human arylamine N-acetyltransferase and U937 cells. , 1995, The Biochemical journal.

[17]  A. Czeizel,et al.  Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. , 1992, The New England journal of medicine.

[18]  M. Gnant,et al.  Prevention of neural tube defects: Results of the Medical Research Council Vitamin Study , 1991, The Lancet.