[extropy-chat] [fwd] Werner's Syndrome Mice
jpnitya at verizon.net
Thu Aug 26 19:22:51 UTC 2004
I've read the paper and these animals do not display such a marked
accelerated aging phenotype as do human patients with WS. Therefore, the
possibility exists that Werner Syndrome mice suffer from accelerated
pathology rather than accelerated aging, a bit like it appears to happen in
the Lamin A mutant mice. The reference for the LMNA mutants:
Nikolova V, et al (2004) Defects in nuclear structure and function promote
dilated cardiomyopathy in lamin A/C-deficient mice. J Clin Invest 113:357-69.
Actually, WRN appears to interact with at least 17 other proteins
(http://genomics.senescence.info/genes/entry.php?id=13). On the issue of
protein interactions and aging, there was a fun paper by Daniel Promislow
arguing that proteins more likely to be involved in aging are the ones with
the higher connectivity--that is, with the higher number of protein-protein
interactions. The reference is:
Promislow DE. Protein networks, pleiotropy and the evolution of senescence.
Proc R Soc Lond B Biol Sci. 2004 Jun 22;271(1545):1225-34.
His ideas are a good complement to my own recent paper:
de Magalhães, JP and Toussaint, O (2004) "GenAge: a genomic and proteomic
network map of human ageing." FEBS Letters 571(1-3):243-247.
Lastly, those of you interested in telomeres and telomerase as a way to
delay aging may be interested in another recent paper of mine:
de Magalhães, JP and Toussaint, O (2004) "Telomeres and telomerase: a
modern Fountain of Youth?" Rejuvenation Research 7:126-132.
All the best,
Joao Pedro de Magalhaes, PhD
Harvard Medical School, Dept. of Genetics
Avenue Louis Pasteur, 77, Room 238
Boston, MA 02115
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