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Gene that governs toxin production in deadly mold found

04-12-2007 · EurekAlert!

For the growing number of people with diminished immune systems -- cancer patients, transplant recipients, those with HIV/AIDS -- infection by a ubiquitous mold known as Aspergillus fumigatus can be a death sentence.

Keywords: gene, governs, toxin, production, deadly, mold, govern

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Snake venoms share similar ingredients
12-19-2007 · EurekAlert!
Venoms from different snake families may have many deadly ingredients in common, more than was previously thought. A study published in the online open access journal BMC Molecular Biology has unexpectedly discovered three-finger toxins in a subspecies of the Massasauga Rattlesnake, as well as evidence for a novel toxin genes resulting from gene fusion.
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Jefferson scientists find protein may be key in developing deadly form of pancreatic cancer
10-11-2007 · EurekAlert!
A tumor-blocking protein previously implicated in prostate and breast cancer development may also be behind the most aggressive type of pancreatic cancer. Researchers have discovered that the protein pp32 -- which normally applies the brakes on a cancer-causing gene -- is missing in an aggressive form of pancreatic cancer. Though the work is preliminary, the scientists say, the absent protein could eventually become a marker for the disease and a potential drug target.
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JCI Table of Contents -- July 2, 2007
07-02-2007 · EurekAlert!
This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, July 2, 2007, in the JCI, including: p53 gene mutations and inflammation trigger skin cancer; Neutrophils stand guard against tuberculosis infection; Mending a broken heart: Dysferlin repairs cardiac cell rupture; Calcium handling and cardiac arrhythmias: how the beat goes on; Hemoglobin production gets a helping hand; Recombinant Hemojuvelin protein: a treatment option for anemia; and others.
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Several genes that regulate the disease SLE have been identified
01-22-2008 · EurekAlert!
Swedish researchers, in collaboration with foreign colleagues, have identified a number of new genes that can be tied to the disease SLE, including a gene that hopefully might be used to treat the disease in the future by regulating the production of antibodies. These unique findings are being published in three articles in the new issue of the journal Nature Genetics.
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Molecule discovered to be key to pain sensitivity
10-22-2006 · EurekAlert!
Sensitivity to pain and the risk of developing chronic pain appear to be influenced by a molecule known to be required for the production of major neurotransmitters. In the November issue of Nature Medicine, an international research team describes this unexpected role for the molecule called BH4 and their findings that a particular set of variations in a human gene involved in synthesizing the molecule, appears to reduce pain sensitivity.
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Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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Green plants share bacterial toxin
11-06-2006 · EurekAlert!
A toxin that can make bacterial infections turn deadly is also found in higher plants, researchers at UC Davis, the Marine Biology Laboratory at Woods Hole, Mass., and the University of Nebraska have found.
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Genome sequencing reveals key to viable ethanol production
03-02-2007 · EurekAlert!
As the national push for alternative energy sources heats up, researchers at the University of Rochester have for the first time identified how genes responsible for biomass breakdown are turned on in a microorganism that produces valuable ethanol from materials like grass and cornstalks.Waste products such as grass clippings and wood chips -- once thought too difficult to turn into ethanol -- may soon be fodder for hungry, gene-tweaked bacteria.
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CU researcher engineers sorghum that grows in poisonous soils
08-27-2007 · EurekAlert!
Aluminum toxicity in acidic soils limits crop production in as much as half the world's arable land. Now, Cornell researchers have cloned a novel aluminum-tolerant gene in sorghum and expect to have genetically engineered aluminum-tolerant sorghum lines by next year.
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University of Washington-led team discovers a gene
12-12-2006 · EurekAlert!
An international group of researchers has discovered that the mutated form of a gene called Palladin causes familial pancreatic cancer. The findings, published online today, Dec. 12, in the peer-reviewed journal PLoS-Medicine, may help explain why the disease is so deadly. The research project was led by Dr. Teri Brentnall, University of Washington associate professor of medicine, and supported by the Lustgarten Foundation, Canary Foundation and other private sources.
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