Literature summary for 3.5.4.36 extracted from

MacGinnitie, A.J.; Anant, S.; Davidson, N.O.
Mutagenesis of apobec-1, the catalytic subunit of the mammalian apolipoprotein B mRNA editing enzyme, reveals distinct domains that mediate cytosine nucleoside deaminase, RNA binding, and RNA editing activity (1995), J. Biol. Chem., 270, 14768-14775.

Search for more literature for 3.5.4.36

Cloned(Commentary)

Cloned (Comment)	Organism
expressed in Escherichia coli, as a glutathione S-transferase fusion protein. Overexpression of wild-type apobec-1 in McA 7777 cells results in a 5-6-fold increase in editing of endogenous apoB	Rattus norvegicus

Protein Variants

Protein Variants	Comment	Organism
C93S	loss of RNA editing activity, great reduction of cytidine deaminase activity	Rattus norvegicus
C96S	wild-type levels of RNA binding, loss of RNA editing activity, great reduction of cytidine deaminase activity	Rattus norvegicus
E63Q	wild-type levels of RNA binding, mutation abolishes both cytidine deaminase and RNA editing activity	Rattus norvegicus
H61C	mutation retains both editing and cytidine deaminase activity	Rattus norvegicus
H61R	mutation abolishes RNA binding, loss of RNA editing activity, great reduction of cytidine deaminase activity	Rattus norvegicus
additional information	mutation of the first four leucines within the heptad repeat of the leucine-rich region (LRR) of apobec-1 results in reduced RNA editing but reservation of wild-type cytidine deaminase activity	Rattus norvegicus
P92L	mutation abolishes both cytidine deaminase and RNA editing activity	Rattus norvegicus

Metals/Ions

Metals/Ions	Comment	Organism	Structure
Zinc	zinc binding is required for both apoB RNA editing and cytidine deaminase activity	Rattus norvegicus

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
intestine	-	Rattus norvegicus	-

Synonyms

Synonyms	Comment	Organism
APOBEC-1	-	Rattus norvegicus
apolipoprotein B mRNA editing enzyme	-	Rattus norvegicus

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Release 2023.1 (January 2023)