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Identification of new genes shows a complex path to cell death

12-14-2007 · EurekAlert!

Researchers at the University of Massachusetts Medical School, gained new insights into autophagy -- a cellular degradation process associated with a form of programmed cell death -- by studying the salivary gland cells of the fruit fly.

Keywords: identification, genes, shows, complex, path, cell, death, gene, show

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Too much sugar turns off gene that controls the effects of sex steroids
11-09-2007 · EurekAlert!
Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, shows a new study in mice and human cell cultures that's published this month in the Journal of Clinical Investigation. This discovery reinforces public health advice to eat complex carbohydrates and avoid sugar.
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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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Brown scientists map structure of DNA-doctoring protein complex
12-06-2006 · EurekAlert!
Mobile DNA, which inserts foreign genes into target cells, is a powerful force in the march of evolution and the spread of disease. Working with the lambda virus and E. coli bacteria, Brown University biologists have solved the structure of a six-protein complex critical to performing this gene-grafting surgery. The technique they developed could be used to reveal the structure of other critical protein complexes, landing the work on the cover of Molecular Cell.
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The importance of gene regulation for common human disease
09-16-2007 · EurekAlert!
A new study published in Nature Genetics on Sunday Sept. 16, 2007, shows that common, complex diseases are more likely to be due to genetic variation in regions that control activity of genes, rather than in the regions that specify the protein code. This surprising result comes from a study at the Wellcome Trust Sanger Institute of the activity of almost 14,000 genes in 270 DNA samples collected for the HapMap Project.
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Children with gene show reduced cognitive function
11-05-2007 · EurekAlert!
Children possessing a gene known to increase Alzheimer's disease risk already show signs of reduced cognitive function, an Oregon Health & Science University study has found. Scientists discovered that 7- to 10-year-olds with a member of a family of genes implicated in development, nerve cell regeneration and neuroprotection display reduced spatial learning and memory, associated with later-life cognitive impairments. This suggests brain changes predisposing a person to Alzheimer's might occur much sooner than previously thought.
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A tricky tumor virus
01-17-2008 · EurekAlert!
Viruses use many tricks to gain control over their host cells and to reprogram them to their own advantage. Dr. Arnd Kieser and his colleagues of the Department of Gene Vectors of the Helmholtz Zentrum Munich, Germany, were able to show in a recent publication in PLoS Biology by which mechanism Epstein-Barr virus exploits a signal protein of its host cell, which normally mediates programmed cell death, in order to convert the cell into a cancer cell.
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2-protein team would be lost without each other
04-19-2007 · EurekAlert!
Just as a hard-charging person sometimes needs a calming partner to be more effective, so it is with a pair of critical proteins that promote cell division and growth in the rapidly expanding root tip of plants. This emerging picture of the complex interplay between genes and proteins is the latest finding to come from Duke University researchers' examination of the model mustard plant Arabidopsis thaliana.
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Bak protein sets stressed cells on suicide path, researchers show
07-12-2007 · EurekAlert!
When a cell is seriously stressed, say by a heart attack, stroke or cancer, a protein called Bak just may set it up for suicide, researchers have found.
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Stem cells show promise for treating Huntington's disease
09-25-2007 · EurekAlert!
Paying close attention to how a canary learns a new song has helped scientists open a new avenue of research against Huntington's disease -- a fatal disorder for which there is currently no cure or even a treatment to slow the disease. Scientists used gene therapy to guide the development of endogenous stem cells in the brains of mice affected by a form of Huntington’s, generating new medium spiny neurons -- the cell lost in Huntington's disease.
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Cancer stem cell marker also drives transcription in normal cells
01-17-2008 · EurekAlert!
New research links the recently discovered function of a multi-faceted transcriptional complex to control of gene expression in both normal cells and cancer stem cells...
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