EC Number   |
Protein Variants |
Reference |
|---|
   2.3.1.22 | more |
MGAT2 knockout mice exhibit a reduction of metabolic efficiency and increased thermogenic energy expenditure when fed a high-fat diet, they are protected from developing obesity, fatty liver, hyperlipidemia, and glucose intolerance despite chronic high-fat feeding |
701625 |
| 2.3.1.22 | more |
mice lacking the gene Mogat2 , which codes for an MGAT highly expressed in the small intestine, are resistant to obesity and other metabolic disorders induced by high-fat feeding. The Mogat2-deficient mice absorb normal amounts of dietary fat but exhibit a reduced rate of fat absorption, increased energy expenditure, decreased respiratory exchange ratio, and impaired metabolic efficiency. Recombinant expression of the human gene MOGAT2, encoding the enzyme, in the intestine increases intestinal MGAT activity, restores fat absorption rate, partially corrects energy expenditure, and promotes weight gain upon high-fat feeding. The changes in respiratory exchange ratio are not reverted, and the recoveries in metabolic efficiency and weight gain are incomplete |
736602 |
| 2.3.1.22 | more |
Mogat2-targeted 129/SvJae embryonic stem cells are generated with a targeting vector designed to replace exon 1 of Mogat2 including the translation-initiating methionine, Mogat2 (-/-) and wild-type are generated from breeding heterozygotes (first backcrossed with C57BL/6J mice) |
705856 |
| 2.3.1.22 | more |
mutant FL-DELTA1-160, with both transmembrane regions deleted, displays relocation in the cytosol. Mutant FL-DELTA161-335, which contains the N-terminus and the two transmembrane domains, exists in the membrane fraction |
756283 |
