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December 12, 2008
PATHOLOGY:
Potentially Universal Mechanism of Aging Discovered
Researchers have uncovered what may be a universal cause of aging, which applies
to both single-cell organisms like yeast and multicellular organisms including
mammals. Their findings, reported in the Nov. 28 Cell, show that DNA
damage eventually leads to a breakdown in the cell’s ability to regulate
which genes are appropriately switched on and off. The study, by Philipp Oberdoerffer
(left), David Sinclair, and colleagues, marks the first time that such an evolutionarily
conserved aging mechanism has been identified in such diverse organisms. It also
introduces hypotheses on how this process might be reversed. |
PROTEOMICS:
Protein Stability Profiling Goes Global
By measuring protein stability on a grand scale, Danny Chou, Stephen
Elledge, Sherry Yen, and Qikai Xu gauged protein levels in the cell that
accounted for both protein synthesis and degradation. Their method is
based on a genetic construct that uses fluorescent red and green proteins
to take measurements on a cellwide scale. The new technique allows researchers
to check the stability of thousands of proteins at the same time to get
a picture of the molecular forces at work in the cell during any given
cell state. The work appears in two papers in the Nov. 7 Science.
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ONCOLOGY:
Unlikely Pair of Mutations Drives Brain Cancer
Some glioblastomas develop slowly while others burst through the
brain so quickly that a person could be healthy one month and gripped by disease
the next. Genetic screens have shown that the faster, or primary, glioblastomas
harbor mutant versions of Pten and other genes. Defects in the well-known
tumor suppressor p53 have been linked almost solely to the slower-growing,
or secondary, glioblastomas. It now appears that corrupted versions of p53 do
play a role in the faster-growing variety, especially when joined by mutant
versions of Pten. From left, Haoqiang Ying, Ronald DePinho, Hongwu
Zheng and colleagues report the findings in the Oct. 23 Nature.
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