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Hello, I'm Kazuko Nishikura,
a professor at the Wistar Institute
in Philadelphia.
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Today, I'm going to
talk about RNA editing.
RNA editing is
a post-transcriptional process that
changes the nucleotide
sequence of an RNA transcript,
resulting in different RNA not
encoded in the genomic DNA.
There are many different types of RNA
editing that modify transcripts of plant,
animal and parasite genomes as
described in Dr Stephen Hajduk's talk.
One particular type of RNA editing
changes adenosine to inosine.
I will talk about this A-to-I RNA editing,
and
especially about its
relevance to human diseases.
ADAR (adenosine deaminase acting
on RNA) is an enzyme involved
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in this A-to-I RNA editing process and
converts adenosine to inosine,
specifically in double-stranded RNAs
through a hydrolytic deamination reaction.
Inosine base-pairs with cytidine and
is treated as
if it were guanosine by
the translation machinery.
Reverse transcriptase also
reads inosine as guanosine,
so A-to-I RNA editing can be detected as
an A-to-G change in the cDNA sequence.
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We identified the first member
of the ADAR gene family ADAR1,
which subsequently led
to identification of two
additional family members,
ADAR2 and ADARs3.
These ADARs are highly
conserved from fish to human.
ADARs share a common
substrate-binding domain containing
two to three repeats of
a double-strand RNA binding motif and
a common deaminase or catalytic domain.
Additional domains
are unique to each member,
such as the Z DNA binding
domain of ADAR1 and
the arginine-lysine-rich single-strand
RNA binding R-domain of ADAR3.
Both ADAR1 and
ADAR2 are detected in many tissues,
whereas ADAR3 is expressed
only in the brain.
