From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Tue Jun 24 2003 - 10:07:30 MDT
On Tue, 24 Jun 2003, Brett Paatsch wrote:
> In the article below it seems the myc cancer causing gene
> (which is already known to be responsible for about a third
> of all cancers (bad gene, very bad! ) produces the protein
> that activates the Werner's gene (a fine friendly gene, one
> warms naturally to it, - because in healthy folk that don't suffer
> from the rare premature aging syndrome known as Werners
> when the gene is broken) it is actually involved in keeping
> cells young and growing.
I think you may be making things overly simple. When the WS
gene is defective, it produces DNA deletions (*that* is very
bad) due to its exonuclease activity (Oshima J et al, Cancer Res
Jan 2002). It appears that p53 is responsible for regulating
the exonuclease activity of the WS protein (Brosh RM, et al
JBC Sep 2001). Now it may be that MYC is upregulating the
production of WRN resulting in a gene dosage imbalance with
p53 that allows the exonuclease activity to proceed when it
is undesirable to do so. But there appear to be other players
since WRN can be phosphorylated at one or more locations.
So I wouldn't point the finger at MYC until it becomes clearer
when WRN is supposed to function as a helicase and when it is
supposed to function as an exonuclease. Before we are done with
this I think we are going to find that exonucleases in general
(WRN, Artemis, etc.) may be an interesting, perhaps even significant,
part of the puzzle.
Robert
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