Literature summary for 1.14.11.54 extracted from

You, C.; Wang, P.; Nay, S.L.; Wang, J.; Dai, X.; OConnor, T.R.; Wang, Y.
Roles of Aag, Alkbh2, and Alkbh3 in the repair of carboxymethylated and ethylated thymidine lesions (2016), ACS Chem. Biol., 11, 1332-1338.

Search for more literature for 1.14.11.54

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q8K1E6	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
MEF cell	-	Mus musculus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
N3-ethylthymidine in mRNA + 2-oxoglutarate + O2	-	Mus musculus	thymidine in mRNA + ?	-	?

Synonyms

Synonyms	Comment	Organism
ALKBH3	-	Mus musculus
alpha-ketoglutarate-dependent dioxygenase alkB homolog 3	-	Mus musculus

General Information

General Information	Comment	Organism
physiological function	the absence of Alkbh3 does not lead to a statistically significant change in the transcriptional blockage or mutagenic properties of O2-ethyl-deoxythymidine, O4-ethyl-deoxythymidine, N3-carboxymethyl-deoxythymidine, and O4-carboxymethyl-deoxythymidine in mammalian cells. N3-ethyl-deoxythymidine induces a substantially higher degree of A to U mutation (about 31%) in Alkbh3-deficient cells than in the wildtype background. N3-ethyl-deoxythymidine, but not other lesions, can be repaired by Alkbh3 in mammalian cells	Mus musculus

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Release 2023.1 (January 2023)