| Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and Abeta Accumulation in Alzheimer's Disease. | Reduction of mNAT1/hNAT2 Contributes to Cerebral Endothelial Necroptosis and Aβ Accumulation in Alzheimer's Disease.
Zou C, Mifflin L, Hu Z, Zhang T, Shan B, Wang H, Xing X, Zhu H, Adiconis X, Levin JZ, Li F, Liu CF, Liu JS, Yuan J. | 11/13/2021 |
| metabolic efficiency in arylamine N-acetyltransferase-deficient mice | A readout of metabolic efficiency in arylamine N-acetyltransferase-deficient mice reveals minor energy metabolism changes.
Denis RGP, Busi F, Castel J, Morel C, Zhang W, Bui LC, Sugamori KS, Prokopec SD, Boutros PC, Grant DM, Rodrigues-Lima F, Luquet S, Dupret JM. | 05/16/2020 |
| these studies demonstrate that Nat1 deletion promotes reduced mitochondrial activity and is associated with ectopic lipid-induced insulin resistance. These results provide a potential genetic link among mitochondrial dysfunction with increased ectopic lipid deposition, insulin resistance, and type 2 diabetes. | Mechanism by which arylamine N-acetyltransferase 1 ablation causes insulin resistance in mice.
Camporez JP, Wang Y, Faarkrog K, Chukijrungroat N, Petersen KF, Shulman GI., Free PMC Article | 07/14/2018 |
| Ca(2+)-dependent N-acyltransferase absolutely required Calcium for its activity and the activity was enhanced by phosphatidylserine. | Phosphatidylserine-stimulated production of N-acyl-phosphatidylethanolamines by Ca(2+)-dependent N-acyltransferase.
Hussain Z, Uyama T, Kawai K, Binte Mustafiz SS, Tsuboi K, Araki N, Ueda N. | 06/2/2018 |
| Nat1 is involved in the translation of proteins that are required for cell differentiation. | Nat1 promotes translation of specific proteins that induce differentiation of mouse embryonic stem cells.
Sugiyama H, Takahashi K, Yamamoto T, Iwasaki M, Narita M, Nakamura M, Rand TA, Nakagawa M, Watanabe A, Yamanaka S., Free PMC Article | 04/14/2018 |
| This study illustrated that deficiency of NAT1/2 decreases isoniazid (INH) acetylation, but increases the interactions of INH with endobiotics in the liver. | Deficiency of N-acetyltransferase increases the interactions of isoniazid with endobiotics in mouse liver.
Wang P, Shehu AI, Lu J, Joshi RH, Venkataramanan R, Sugamori KS, Grant DM, Zhong XB, Ma X., Free PMC Article | 12/9/2017 |
| our results suggest that Nat1 deficiency results in mitochondrial dysfunction, which may constitute a mechanistic link between this gene and insulin resistance . | Nat1 Deficiency Is Associated with Mitochondrial Dysfunction and Exercise Intolerance in Mice.
Chennamsetty I, Coronado M, Contrepois K, Keller MP, Carcamo-Orive I, Sandin J, Fajardo G, Whittle AJ, Fathzadeh M, Snyder M, Reaven G, Attie AD, Bernstein D, Quertermous T, Knowles JW., Free PMC Article | 12/2/2017 |
| Differences between murine arylamine N-acetyltransferase type 1 and human arylamine N-acetyltransferase type 2 defined by substrate specificity and inhibitor binding.( | Differences between murine arylamine N-acetyltransferase type 1 and human arylamine N-acetyltransferase type 2 defined by substrate specificity and inhibitor binding.
Laurieri N, Kawamura A, Westwood IM, Varney A, Morris E, Russell AJ, Stanley LA, Sim E., Free PMC Article | 08/8/2015 |
| In adipocytes, Nat1 silencing lowered insulin-mediated glucose uptake, raised lipolysis, and decreased differentiation. Overexpression did the opposite. Nat1(-) mice had high fasting blood glucose, insulin, and triglycerides and low insulin sensitivity. | Identification and validation of N-acetyltransferase 2 as an insulin sensitivity gene.
Knowles JW, Xie W, Zhang Z, Chennamsetty I, Assimes TL, Paananen J, Hansson O, Pankow J, Goodarzi MO, Carcamo-Orive I, Morris AP, Chen YD, Mäkinen VP, Ganna A, Mahajan A, Guo X, Abbasi F, Greenawalt DM, Lum P, Molony C, Lind L, Lindgren C, Raffel LJ, Tsao PS, RISC (Relationship between Insulin Sensitivity and Cardiovascular Disease) Consortium, EUGENE2 (European Network on Functional Genomics of Type 2 Diabetes) Study, GUARDIAN (Genetics UndeRlying DIAbetes in HispaNics) Consortium, SAPPHIRe (Stanford Asian and Pacific Program for Hypertension and Insulin Resistance) Study, Schadt EE, Rotter JI, Sinaiko A, Reaven G, Yang X, Hsiung CA, Groop L, Cordell HJ, Laakso M, Hao K, Ingelsson E, Frayling TM, Weedon MN, Walker M, Quertermous T., Free PMC Article | 07/4/2015 |
| Transfection assays in mice using hydrodynamics-based procedure and reporter gene assay in a mouse cell line revealed that glucocorticoid-induced NAT gene expression is species dependent | Glucocorticoid receptor-mediated transcriptional regulation of N-acetyltransferase 1 gene through distal promoter.
Bonamassa B, Ma Y, Liu D., Free PMC Article | 10/27/2012 |
| NAT1 affects cell growth and morphology | RNAi-mediated knock-down of arylamine N-acetyltransferase-1 expression induces E-cadherin up-regulation and cell-cell contact growth inhibition.
Tiang JM, Butcher NJ, Cullinane C, Humbert PO, Minchin RF., Free PMC Article | 04/7/2012 |
| Biochemical analysis demonstrated that mNAT1 and its evolutionarily conserved co-subunit, mARD1, assemble to form a functional acetyltransferase. | An evolutionarily conserved N-terminal acetyltransferase complex associated with neuronal development.
Sugiura N, Adams SM, Corriveau RA. | 01/21/2010 |
| Results suggest that peroxynitrite-dependent inactivation of NAT1 and 2 may contribute to muscle dysfunction by impairing the biotransformation activity of this key cellular defense enzyme system. | Impairment of the activity of the xenobiotic-metabolizing enzymes arylamine N-acetyltransferases 1 and 2 (NAT1/NAT2) by peroxynitrite in mouse skeletal muscle cells.
Dairou J, Dupret JM, Rodrigues-Lima F. | 01/21/2010 |
| identification and functional characterization of novel polymorphisms in mice | Identification and functional characterization of novel polymorphisms associated with the genes for arylamine N-acetyltransferases in mice.
Boukouvala S, Price N, Sim E. | 01/21/2010 |