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IN THIS ISSUE . . .
November 15, 2005
Check out the new Biomedical Beat Cool Image
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The National Institute of General Medical Sciences (NIGMS),
one of the National Institutes of Health, supports all research
featured in this digest. Although only the lead scientists
are named, coworkers and other collaborators also contributed
to the findings. To read additional news items, visit NIGMS
News.
Cool Image: Natural Nanomachine in Action
Using a supercomputer to simulate the movement of atoms
in a ribosome, researchers looked into the core of this
protein-making nanomachine and took snapshots. The picture
shows an amino acid (green) being delivered by transfer
RNA (yellow) into a corridor (purple) in the ribosome. In
the corridor, a series of chemical reactions will string
together amino acids to make a protein. The research project,
which tracked the movement of more than 2.6 million atoms,
was the largest computer simulation of a biological structure
to date. The results shed light on the manufacturing of
proteins and could aid the search for new antibiotics, which
typically work by disabling the ribosomes of bacteria. Courtesy
of Kevin Sanbonmatsu, a computational structural biologist
at the Los Alamos National Laboratory.
Full
story
Sanbonmatsu
lab home page
Article
abstract (from the November 1, 2005 issue of PNAS)
Rogue Protein Clumps Kill Brain Cells in Lou
Gehrig’s Disease
Scientists have observed that a hallmark of many brain-wasting
diseases is the presence of protein clumps inside brain cells.
Among people with the devastating neurodegenerative disorder
called amyotrophic lateral sclerosis, or Lou Gehrig’s
disease, 10 percent have an inherited form that’s caused
by an error in the gene SOD1. While researchers know that
this genetic misstep causes cells to make SOD1 proteins that
don’t fold properly and form clumps, no one has proven
that the clumping of the proteins is what causes neuronal
cell death associated with Lou Gehrig’s disease. Using
time-lapse microscopy to watch living brain cells one at a
time, molecular biologist Richard Morimoto of Northwestern
University has revealed that only cells containing rogue SOD1
protein clumps died. This finding helps explain how the disease
occurs and could point the way to new treatment approaches.
Full
story
Morimoto
lab
Article
abstract (from the October 10, 2005 issue of the Journal
of Cell Biology)
Computer Models Show Dengue Virus in Catch-22
for Survival
Many viruses exploit the human body’s immune system
to increase their replication and infect more people. But
this ability also may be the downfall of some viruses, according
to new computer models developed by infectious disease scientists
Derek Cummings and Donald Burke of the Johns Hopkins Bloomberg
School of Public Health. The models simulate the dynamic role
that a process called antibody-dependent enhancement plays
in the spread of the dengue virus, which annually infects
millions of people worldwide. In the simulation, antibody-dependent
enhancement allowed the virus to grow faster in people who
had been previously infected and as a result had partial immunity
to the virus. But faster growth triggered a more lethal form
of the disease that led to more deaths and ultimately the
extinction of the virus. The models may apply to other diseases
in which partial immunity increases viral replication and
could help inform the design and development of effective
dengue vaccines.
Full
story
Burke
home page
Article
abstract (from the October 18, 2005, issue of PNAS)
Researchers Uncover New Role for DNA-Packaging
Molecule
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Caption: Each spot of this microarray grid represents
Htz1 presence at a specific segment of DNA that
governs the activity of nearby genes. Htz1 is highly
present in red spots, while it has moderate and
low presence in the yellow and green spots, respectively.
Htz1 loss is associated with gene activation. Courtesy
of Bradley Cairns.
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To understand why certain genes turn on or off in cancer
cells, researchers must first figure out what’s happening
inside normal cells. New findings from cancer biologist
Bradley Cairns of the University of Utah offer some insight.
The DNA in chromosomes is wrapped around cellular bobbins
called nucleosomes, which package the genetic material into
a compact form. While scientists knew that the components
of the nucleosome could vary, they were unsure what effects
these variations could have on gene activation. But then
Cairns discovered a key switch in certain genes—a
nucleosome component called Htz1. When present, Htz1 keeps
nearby genes off or repressed. But when it’s ejected,
the same genes turn on. The results show that this variation
in the nucleosome does in fact make fundamental contributions
to regulating gene activity.
Full
story
Cairns
home page
Article
abstract (from the October 21, 2005, issue of Cell)
How Genes Affect Drug Responses: 5 Years of Discovery
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Caption: Green shows transporter proteins embedded
in cell membranes. Transporter proteins in the liver
and kidney purge drugs and other chemicals from
the body. Genetic variations in these proteins can
change how a person responds to medications. Provided
by Kathy Giacomini. Copyright 2003 National Academy
of Sciences, U.S.A.
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Medicines that work wonders for some people can be ineffective
or even toxic to others. To understand how genetic variations
affect the way a person responds to medicines and to help
doctors prescribe the drugs and dosages that work best for
each person, NIGMS led the creation of a nationwide NIH
Pharmacogenetics Research Network in 2000. Scientists in
the network have greatly advanced the understanding of genes
and medications related to asthma, heart disease, depression,
cancer, and other health disorders. Kathleen M. Giacomini,
a pharmacologist at the University of California, San Francisco,
uncovered more than a thousand variants in cellular “gatekeeper”
molecules called transporters. She is now studying how these
genetic variants affect people’s responses to the
antidepressants Paxil® and Prozac®. Scott Weiss,
a research physician at Brigham and Women's Hospital and
Harvard Medical School, has identified and is developing
prototype tests to detect gene variants that affect the
way people respond to asthma medicines. More examples are
available at the link below.
Full
story
PGRN
home page
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