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HFI-1 gene has key role in both oxygen sensing, heat shock pathway

10-25-2006 · EurekAlert!

University of Oregon researchers have found an unexpected regulatory link between cellular responses to hypoxia and heat shock. Central to the discovery is a gene known as Hypoxia-Inducible Factor-1 that is critical for both normal and pathological changes, making it a potential target for both health promotion and cancer therapies.

Keywords: hfi-1, gene, key, role, oxygen, sensing, heat, shock, pathway, hfi

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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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Gene-bender proteins may sway to DNA
12-04-2006 · EurekAlert!
Using a technique called laser temperature-jump, biophysicist Anjum Ansari and her colleagues have made the first direct observation of DNA bending when bound to a DNA-bending protein. DNA bending plays a key role in regulating gene expression, and better understanding of the process may help in developing gene-based therapies.
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Naked mole-rats bear chili pepper heat
01-28-2008 · EurekAlert!
Scientists have used gene therapy to restore sensation in naked mole-rats, strange rodents that lack a key neurotransmitter that causes prolonged pain perception in other mammals. The finding may lead to new analgesics for people with chronic pain who do not respond to current medication.
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Gene found for rare disorder may reveal new pathway in mental retardation
02-05-2007 · EurekAlert!
Studying mutations that give rise to a rare genetic disease, genetics researchers have identified a novel biological pathway that may have a broader role during human development, potentially in cases of mental retardation and autism. An international team of researchers identified two genes that contribute to Cornelia deLange syndrome, a multisystem genetic disease that affects an estimated one in 10,000 children.
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Study reveals a key to blood vessel growth and possible drug target
10-14-2007 · EurekAlert!
Researchers have identified a molecular pathway that plays a critical role in the growth of blood vessels. The finding not only offers an important insight into the development of the vascular system during embryonic development but suggests a potential target for inhibiting the blood vessels that fuel cancers, diabetic eye complications and atherosclerosis, the researchers say.
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Scientists unlock mystery of embryonic stem cell signaling pathway
03-19-2007 · EurekAlert!
A newly discovered small molecule called IQ-1 plays a key role in preventing embryonic stem cells from differentiating into one or more specific cell types, allowing them to instead continue growing and dividing indefinitely, according to research performed by a team of scientists who have recently joined the stem-cell research efforts at the Keck School of Medicine of the University of Southern California.
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Gene therapy for blindness clears hurdle in mice
03-14-2007 · EurekAlert!
University of Florida Genetics Institute researchers were able to use interfering RNA in experiments with mice to quiet a gene that plays a crucial role in a leading cause of inherited blindness. Disabling the gene is a step toward developing a gene therapy to treat people with retinitis pigmentosa, an inherited disease that attacks the light-sensing cells in the eye.
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New pathway provides more clues about BRCA1 role in breast cancer
01-15-2008 · EurekAlert!
A breast cancer gene's newly discovered role in repairing damaged DNA may help explain why women who inherit a mutated copy of the gene are at increased risk for developing both breast and ovarian cancer.
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Scientists discover way to block growth of prostate cancer cells
11-08-2006 · EurekAlert!
Scientists have discovered for the first time a specific biochemical pathway by which the sex hormone, androgen, increases levels of harmful chemicals called reactive oxygen species (ROS) in the prostate gland that play a role in the development of prostate cancer, the 18th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics in Prague heard on Wednesday.
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Scientists map key landmarks in human genome
01-16-2007 · EurekAlert!
Dana-Farber Cancer Institute researchers have developed a powerful method for charting the positions of key gene-regulating molecules called nucleosomes throughout the human genome. The mapping tool could help uncover important clues for understanding and diagnosing cancer and other diseases, the scientists say. Moreover, it may shed light on the role of nucleosomes in the process of "reprogramming" an adult cell to its original embryonic state, which is a critical operation in cloning.
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