Literature summary for 2.3.1.5 extracted from

Wakefield, L.; Long, H.; Lack, N.; Sim, E.
Ocular defects associated with a null mutation in the mouse arylamine N-acetyltransferase 2 gene (2007), Mamm. Genome, 18, 270-276.

Search for more literature for 2.3.1.5

Application

Application	Comment	Organism
medicine	ocular defects associated with a null mutation in the mouse arylamine N-acetyltransferase 2 gene	Mus musculus

Protein Variants

Protein Variants	Comment	Organism
additional information	the developmental role of Nat2 is investigated using transgenic Nat2 knockout/lacZ knockin mice: The transgene is bred onto an A/J background and offspring are scored for developmental defects at weaning. After backcross generation eight, an ocular defect, ranging from cataract to microphthalmia and anophthalmia, is recorded among offspring of backcross and intercross pairs. While Nat2-/- mice are described as overtly aphenotypic, the presence of a Nat2 null allele in one or both parents can result in ocular defects. These ocular phenotypes and their association with Nat2 genotype indicate that the Nat2 locus may be responsible for the described microphthalmic phenotype	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
eye	-	Mus musculus	-
neural tube	-	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
arylamine N-acetyltransferase 2	-	Mus musculus
NAT2	-	Mus musculus

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Release 2023.1 (January 2023)