Daily non-political popular news in brief.

New study shows how genetic repair mechanism helps seal DNA breaks

10-19-2006 · EurekAlert!

A new study by researchers from the Scripps Research Institute, Lawrence Berkeley National Laboratory, the Washington University School of Medicine and the University of Maryland has provided a clearer picture of the final steps of a critical DNA repair process. When these repair processes go awry, cells can malfunction, die or become cancerous.

Keywords: study, shows, genetic, repair, mechanism, seal, dna, breaks, show, break

« Previous | Next »

Similar news on "New study shows how genetic repair mechanism helps seal DNA breaks":

Genetic repair mechanism clears the way for sealing DNA breaks
10-19-2006 · EurekAlert!
Scientists investigating an important DNA-repair enzyme now have a better picture of the final steps of a process that glues together, or ligates, the ends of DNA strands to restore the double helix.
Similar news · Read more »
Unknotting DNA clue to cancer syndrome
08-02-2007 · EurekAlert!
A new UC-Davis study that explains the actions of a gene mutation that causes early onset cancer provides a fundamental insight into the mechanism of DNA-break repair.
Similar news · Read more »
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.
Similar news · Read more »
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.
Similar news · Read more »
Identifying the mechanism behind a genetic susceptibility to type 2 diabetes
08-01-2007 · EurekAlert!
Type 2 diabetes is reaching epidemic proportions in the developed world. Determining if and how certain genes predispose individuals to type 2 diabetes is likely to lead to the development of new treatment strategies for individuals with the disease. A new study now shows that certain variants of the gene TCF7L2 make individuals more susceptible to type 2 diabetes and provides a mechanism by which these genetic variants might cause susceptibility to the disease.
Similar news · Read more »
Novel MS drug shows promise in 2 lethal leukemias
08-28-2007 · EurekAlert!
A new study suggests that an experimental drug being tested for the treatment of multiple sclerosis and to prevent organ rejection might also help people with certain deadly forms of chronic and acute leukemia. The laboratory and animal study focused on the drug, called fingolimod. Researchers said it might help patients with advanced chronic myelogenous leukemia or acute lymphocytic leukemia, and whose cancer cells show a particular genetic change called the Philadelphia chromosome.
Similar news · Read more »
Scientists show that mitochondrial DNA variants are linked to risk factors for type 2 diabetes
08-10-2007 · EurekAlert!
Researchers report for the first time that genetic variants in mitochondria -- energy-producing structures harboring DNA that are inherited only from the mother -- are directly linked to metabolic markers for type 2 diabetes. The study, which highlights the role of mitochondrial genome variation in the pathogenesis of common diseases, is published online in Genome Research.
Similar news · Read more »
Penn researchers discover new mechanism for viral replication
08-16-2007 · EurekAlert!
Researchers have identified a new strategy that Kaposi's Sarcoma Associated Herpesvirus uses to dupe infected cells into replicating its viral genome. This is the first study to directly show that a section of viral DNA can independently draw upon proteins within a host cell to promote its own replication.
Similar news · Read more »
Enhanced DNA-repair mechanism can cause breast cancer
10-15-2007 · EurekAlert!
Although defects in the "breast cancer gene," BRCA1, have long been known to increase the risk for breast cancer, exactly how the defects lead to tumor growth has remained a mystery. Now scientists provide insight into how the normal BRCA1 gene suppresses the growth of tumors as well as the nature of the genetic instability that leads to cancer when BRCA1 is defective.
Similar news · Read more »
DNA repair proteins monitored at double-strand break
05-09-2007 · EurekAlert!
Investigators at St. Jude Children's Research Hospital had a molecule’s eye view of the human cell’s DNA repair kit as it assembled on a double-strand break to link together the broken ends. Double-strand breaks are ruptures that cut completely across the twisted, ladder-like structure of DNA, breaking it into two pieces.
Similar news · Read more »