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splicing. These results indicate that the CTD of RNA pol II is required to
coordinate editing and splicing, possibly through delaying the splicing event
until editing has occurred thereby allowing these processes to occur sequentially.
XVII. CONCLUSION
Despite it being approximately 20 years since ADARs were first identified, many
questions still remain unanswered. One of the main challenges is to identify the
function of ADAR1. Is it an RNA-editing enzyme and if so what are its
substrates? Recent publications suggest that instead it may play an important
role in the interferon response particularly during embryogenesis in the liver.
What is the function of ADAR3 and TENR both of which are evolutionarily
conserved but catalytically inactive? Another question is what is the relationship
between ADARs and RNA interference? Is there an important miRNA, similar
to the
site that requires editing or do ADARs instead edit the
miRNA target sequences in the 5
0
- and 3
0
-UTRs? The question that still remains
a challenge to answer is why is there editing of the Q/R site in
GluR-B Q/R
? Why is it
not genomically encoded if editing at this position is critical for the functioning
of the AMPA receptor and failure of editing can lead to neuronal cell death?
These and other mysteries remain to be addressed.
GluR-B
Acknowledgments
Some of the material for this chapter was taken from the PhD thesis of Marion Hogg. We would like
to thank Craig Nicols for his help with figures. M. A. O. C. is funded by the Medical Research
Council Grant U.1275.01.005.00001.01.
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