A once-a-month electronic newsletter ofbasic, preclinical and translational
research news from the Johns Hopkins School of Medicine. Please forward
freely. Browse back issues of the e-Newsletter in the archive.
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RESEARCH HIGHLIGHTS:
- Cutting Off Gene Expression
- Mutating A Mutant For A Cure?
- Hope For New Anti-Malarial Drugs
- What Flies Can Teach Us About Caffeine
NEWS BRIEFS:
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Do you have a manuscript in press? Fax your manuscript or galley proofs to
Media Relations and Public Affairs at 410-614-8951, or e-mail the appropriate
media relations person.
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RESEARCH HIGHLIGHTS:
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9/15/06
Cutting Off Gene Expression
So-called cryptic unstable transcripts – known as CUTs -- are tiny bits of RNA that are transcribed from stretches of DNA that do not appear to be functional genes. In yeast, CUTs – whose presence could pose danger to the cells -- are made for reasons unclear and are degraded rapidly by machinery in the nucleus called the nuclear exosome. Jeffry Corden and colleagues in molecular biology and genetics now have found that two genes, known as Nrd1 and Nab3, are responsible for properly terminating CUTs before they get too long. The Nrd1 and Nab3 proteins bind to regions along the chromosomes where CUTs are being made, and mutants in Nrd1 and Nab3 make longer, readthrough CUTs that are not properly degraded. This recent work reveals that Nrd1 and Nab3 stop short the transcription of these tiny RNAs and signal their presence to the nuclear exosome, which gets rid of the nonsense CUTs.
Read the paper here.
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9/17/06
Mutating The Mutant For A Cure?
Some mutations are worse than others. One particular mutation is the culprit behind 5 percent to 6 percent of inherited, dominant Parkinson disease as well as 1 percent to 2 percent of the form that is not inherited, the so-called sporadic Parkinson disease. This particular mutation in an enzyme known as LRKK2 causes it to be more active than usual. The hyperactive LRKK2 causes the nerve-cell death and brain degeneration associated with both the inherited and non-inherited forms of Parkinson. Researchers in Hopkins’ Institute for Cell Engineering, neurobiology, neurology and neuroscience now have identified other mutations in LRKK2 that appear to counteract the hyperactive mutation that causes nerve cells to die. By turning down the enzyme, the newly identified mutations might provide targets for designing new drugs and therapies for Parkinson disease.
Read the paper here.
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9/18/06
Hope For New Anti-Malarial Drugs
One of the most difficult aspects of drug design is finding a molecule that does what it’s supposed to do – kill the pesky microbe – without hurting the host. Now, after searching through a collection of 175,000 chemicals, a research team in pharmacology and molecular sciences led by Jun Liu has found a whole family of chemicals that can inhibit a malaria-specific enzyme called MetAP, short for methionine aminopeptidase. The newly discovered chemicals stop malaria – both drug-sensitive and drug-resistant – in infected mice, prolonging their survival. Dosing twice a day cured 60 percent of infected mice. When tested on mice infected with drug-resistant malaria, the new chemical cured 80 percent of the mice. When used in combination with chloroquine – the current treatment for malaria -- all infected mice were cured. Chloroquine treatment alone cured only 40 percent of infected mice. Using chemistry, Liu and his team hope to tweak the new chemicals to improve their potency in mice before they consider similar experiments in people.
Read the paper here.
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9/18/06
What Flies Can Teach Us About Caffeine
Flies drink coffee? Well, normally they don’t because they avoid bitter-tasting compounds. However, it turns out that flies that can’t taste the bitterness of caffeine will drink it up. Craig Montell and colleagues in biological chemistry have identified a mutation in the taste receptor gene Gr66a of fruit flies that both prevents them from tasting bitterness and obliterates their ability to sense caffeine. This taste receptor gene is responsible for the bitter response in tea but not for the one in chocolate.
Read the press release here:
Read the paper here:
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NEWS BRIEFS:
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Carol Greider Wins Lasker Award
Last week, Carol Greider and her family traveled to New York City to receive the 2006 Albert Lasker Award for Basic Medical Research at a special award luncheon. Along with Elizabeth H. Blackburn, Ph.D., of the University of California, San Francisco, and Jack Szostak, Ph.D., of Harvard Medical School, Greider was recognized for her discovery of telomerase, an enzyme that maintains the length and integrity of chromosome ends (telomeres) and has drawn intense interest from researchers studying the role of telomeres in everything from aging to cancer.
Read the press release here:
Watch a video interview of Carol Lasker here:
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ICE Fellow Wins Peter Gruber International Research Award in Neuroscience
Saskia Biskup, a postdoctoral fellow in Ted Dawson’s laboratory studying the gene responsible for late-onset autosomal-dominant Parkinson disease, will be awarded the Peter Gruber International Research Award in Neuroscience at the upcoming Society for Neuroscience annual meeting this month in Atlanta, Ga. The Peter Gruber International Research Award in Neuroscience honors young scientists studying at an institution located in a country other than where they hold citizenship or permanent residency. Biskup hails from Germany and is “very happy to be here,” she says. “It is a great experience to work in such a wonderful research environment.”
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Save the Date: Nov. 13 Center for Sensory Biology Inaugural Symposium
The Center for Sensory Biology Inaugural Symposium
“Sensory Biology: Understanding Our Windows to the World”
8:30 a.m. to 5 p.m., Monday, Nov. 13, 2006
Vernon B. Mountcastle Auditorium
Johns Hopkins School of Medicine
725 N. Wolfe St.
Baltimore, MD 21205
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Find Change and Basics online from a Hopkins computer.
Visit Research WebNotes online.
Read Hopkins press releases online.
Upcoming lectures and seminars are listed on the Science Calendar.
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-- JHM --
