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Archive - Dec 2012

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December 5th

Nuclear Import of Transcriptional Repressor in Jasmonate Signaling

Researchers examining how the hormone jasmonate works to protect plants and promote their growth have discovered how a transcriptional repressor of the jasmonate signaling pathway makes its way into the nucleus of the plant cell. The scientists hope that this recently published discovery will eventually help farmers experience better crop yields with less use of potentially harmful chemicals. “This is a small piece of a bigger picture, but it is a very important piece,” said Dr. Maeli Melotto, a University of Texas at Arlington (UT Arlington) assistant professor of biology. Dr. Melotto recently co-authored a paper that advances current understanding of plant defense mechanisms with her collaborator Dr. Sheng Yang and his team at Michigan State University’s Department of Energy Plant Research Laboratory (DOE-PRL). Dr. Yeng is a Howard Hughes Medical Institute-Gordon and Betty Moore Foundation investigator. The collaborative paper was published in the December 4, 2012 issue of PNAS. Jasmonate signaling has been a target of intense research because of its important role in maintaining the balance between plant growth and defense. In healthy plants, jasmonates play a role in reproductive development and growth responses. But, when stressors such as herbivorous insects, pathogen attack, or drought come into play, jasmonate signaling shifts to defense-related cellular processes. The team from UT Arlington and Michigan State focused on the role of jasmonate signaling repressors referred to as JAZ. Specifically, the scientists looked at how JAZ interacts with a major transcription factor called MYC2 and a protein called COI1, which is a receptor necessary for jasmonate signaling.

Novel Drug Reduces Depression Scores within Hours in Phase IIa Trial

Naurex Inc., a clinical stage company developing innovative treatments to address unmet needs in psychiatry and neurology, today reported positive results from a Phase IIa clinical trial of its lead antidepressant compound, GLYX-13. GLYX-13 is a novel partial agonist of the NMDA receptor. The Phase Ila results are being presented at the 51st Annual Meeting of the American College of Neuropsychopharmacology (ACNP), being held December 2-6, 2012 in Hollywood, Florida. The Phase IIa results show that a single administration of GLYX-13 produced statistically significant reductions in depression scores in subjects who had failed treatment with one or more antidepressant agents. The reductions were evident within 24 hours and persisted for an average of seven days. Importantly, the effect size, a measure of the magnitude of the drug's antidepressant efficacy, observed at 24 hours and at seven days after a single administration of GLYX-13, was nearly double the effect size seen with most other antidepressant drugs after 4-6 weeks of repeated dosing. In the Phase IIa trial, GLYX-13 was well tolerated. Reported side effects were mild to moderate and were consistent with those observed in subjects receiving placebo. Consistent with previous studies, GLYX-13 did not produce any of the schizophrenia-like psychotomimetic effects associated with other drugs that modulate the NMDA receptor. "These data are an important step in validating Naurex's mission of developing breakthrough therapies for depression and other CNS disorders," said Derek Small, CEO of Naurex. "Our founder discovered a new class of drugs that appeared to have the remarkable antidepressant efficacy of ketamine-like compounds, but without their limiting side effects.

December 5th

X-Ray Laser Reveals Structure of Key Sleeping Sickness Enzyme

An international team of scientists, using the world’s most powerful X-ray laser, has revealed the three-dimensional structure of a key enzyme that contributes to the pathogenicity of the single-celled parasite that causes African trypanosomiasis (or sleeping sickness) in humans. With the elucidation of the 3D structure of the cathepsin B enzyme, it should be possible to design new drugs to inhibit the parasite (Trypanosoma brucei) that causes sleeping sickness, leaving the infected human unharmed. The research team, including several Arizona State University (ASU) scientists, was led by the German Electron Synchrotron (DESY) scientist Dr. Henry Chapman from the Center of Free-Electron Laser Science (CFEL), professor Christian Betzel from the University of Hamburg and Dr. Lars Redecke from the SIAS joint Junior Research Group at the Universities of Hamburg and Lübeck. The team reported its findings on November 29, 2012 in Science. "This is the first new biological structure solved with a free-electron laser," said Dr. Chapman of the development. "These images of an enzyme, which is a drug target for sleeping sickness, are the first results from our new ‘diffract-then-destroy’ snapshot X-ray laser method to show new biological structures which have not been seen before,” explained Dr. John Spence, ASU Regents’ Professor of Physics. “The work was led by the DESY group and used the Linac Coherent Light Source at the U.S. Department of Energy’s SLAC National Accelerator Laboratory." Transferred to its mammalian host by the bite of the tsetse fly, the effects of the parasite are almost always fatal if treatment is not received. The sleeping sickness parasite threatens more than 60 million people in sub-Saharan Africa and annually kills an estimated 30,000 people.