Researchers have created a model that may explain the complexities of the origins of life. Their work offers new insights into how RNA signaling likely developed into the modern “genetic code.”
Researchers have tied mutations in a gene that causes amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders to the toxic buildup of certain proteins and related molecules in cells, including neurons.
Joslin scientists, in collaboration with researchers from the Harvard School of Public Health and Italian research institutes, have identified a previously unknown genetic variant associated with an increased risk of coronary heart disease (CHD) in type 2 diabetic patients. This discovery has the potential to lead to the development of new treatments for CHD in diabetic patients.
By creating a powerful new gene regulation system called CRISPR-on, Whitehead Institute researchers now have the ability to increase the expression of multiple genes simultaneously and precisely manipulate each gene’s expression level. The system is effective in both mouse and human cells as well as in mouse embryos.
Scientists successfully crystallized a short RNA sequence, poly (rA)11, and used data collected at the Canadian Light Source (CLS) and the Cornell High Energy Synchrotron to confirm the hypothesis of a poly (rA) double-helix.
Of the over 1,900 errors already reported in the gene responsible for cystic fibrosis (CF), it is unclear how many of them actually contribute to the inherited disease. Now a team of researchers reports significant headway in figuring out which mutations are benign and which are deleterious, accounting for 95 percent of the variations found in patients with CF.
In an era of widespread genetic sequencing, the ability to edit and alter an organism’s DNA is a powerful way to explore the information within and how it guides biological function.
A new study has revealed marked differences in the genomic terrain of the two most common types of cervical cancer, suggesting that patients might benefit from therapies geared to each type’s molecular idiosyncrasies.
A statistical model accounting for dozens of different genes in combination—and the interactions between them—is an important step forward in understanding the genetic factors affecting the risk of Crohn's disease (CD), reports a study in Inflammatory Bowel Diseases, official journal of the Crohn's & Colitis Foundation of America (CCFA). The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.
Researchers from Beth Israel Deaconess Medical Center and Boston University School of Medicine find that the same genetic mutation responsible for red hair also promotes a well-known cancer-causing pathway
High-risk pregnant women are being recruited for a clinical trial that aims to give parents detailed information about genetic abnormalities found with the latest prenatal genetic testing, known as microarray.
By any measure, tuberculosis (TB) is a wildly successful pathogen. It infects as many as two billion people in every corner of the world, with a new infection of a human host estimated to occur every second.
A rare, small RNA turns a gene-splicing machine into a switch that controls the expression of hundreds of human genes. Researchers have discovered an entirely new aspect of the gene-splicing process that produces messenger RNA.
Part of the risk for alcohol dependence is genetic. The same is true for eating disorders. Now researchers at Washington University School of Medicine in St. Louis have found that some of the same genes likely are involved in both. They report that people with alcohol dependence may be more genetically susceptible to certain types of eating disorders and vice versa.
Researchers have found and cloned a gene that prevents wheat from preharvest sprouting. The finding will to be most beneficial to white wheat production, which loses $1 billion annually.
By directly altering the gene coding for the prion protein (PrP), Whitehead Institute researchers have created mouse models of two neurodegenerative prion diseases, each of which manifests in different regions of the brain. These new models for fatal familial insomnia (FFI) and Creutzfeldt-Jakob disease (CJD) accurately reflect the distinct patterns of destruction caused by the these diseases in humans. Remarkably, as different as each disease is, they both spontaneously generate infectious prions.
Placentas support the fetus and mother, but those organs grow according to blueprints from dad, according to new research at Cornell University. The study, published in the Proceedings of the National Academy of Sciences in June, shows that the genes in a fetus that come from the father dominate in building the fetal side of the placenta.
Research led by scientists from the University of California, San Diego has decoded the genetic basis of chronic mountain sickness (CMS) or Monge’s disease. Their study provides important information that validates the genetic basis of adaptation to high altitudes, and provides potential targets for CMS treatment.
A multi-institutional team led by Dianna Milewicz, M.D., Ph.D., of The University of Texas Health Science Center at Houston (UTHealth) has found a recurrent genetic mutation that has been linked to deadly thoracic aortic dissections in family members as young as 17 years of age.
A gene variant strongly associated with development of type 2 diabetes appears to interact with a Mediterranean diet pattern to prevent stroke, report researchers from Tufts University and from Spain. The results are a significant advance for nutrigenomics, the study of the linkages between nutrition and gene function.
Researchers have probed deep into the cell’s genome, beyond the basic genetic code, to begin learning the “grammar” that helps determine whether or not a gene gets switched on to make the protein it encodes.
Neurologists and epilepsy researchers from NYU Langone Medical Center were among scientists who have 329 random genetic mutations associated with two of the most severe forms of epilepsy, according to a paper published today in Nature. Though well-known that many forms of epilepsy are strongly influenced by genetics, there has been relatively little progress in identifying the genetic differences that contribute to most forms of epilepsy.
A decade ago, gene expression seemed so straightforward: genes were either switched on or off. Not both. Then in 2006, a blockbuster finding reported that developmentally regulated genes in mouse embryonic stem cells can have marks associated with both active and repressed genes, and that such genes, which were referred to as “bivalently marked genes”, can be committed to one way or another during development and differentiation.
Researchers have identified two new genes and implicated 25 distinct mutations in serious forms of epilepsy, suggesting a new direction for developing tailored treatments of the neurological disorders.
The findings by an international research collaboration, which includes investigators from Duke Medicine, appear Aug. 11 in the journal Nature.
Genomic sequencing experts at Johns Hopkins partnered with pharmacologists at Stony Brook University to reveal a striking mutational signature of upper urinary tract cancers caused by aristolochic acid, a plant compound contained in herbal remedies used for thousands of years to treat a variety of ailments such as arthritis, gout and inflammation. Their discovery is described in the Aug. 7 issue of Science Translational Medicine.
Researchers at the University of California, San Diego School of Medicine offer an explanation for why we all don't get Alzheimer's disease (AD) - a trick of nature that in most people maintains critical separation between a protein and an enzyme that, when combined, trigger the progressive cell degeneration and death characteristic of AD.
A collaborative team of researchers including scientists from UCLA has uncovered evidence that a specific genetic alteration appears to contribute to schizophrenia. They also found that schizophrenia shares a common biological pathway with Fragile X mental retardation syndrome.
A study by Valentina Moskvina, Ph.D., of the Cardiff University School of Medicine, Wales, United Kingdom, and colleagues, examined the genetic overlap between Parkinson disease (PD) and Alzheimer disease (AD).
An experimental treatment for alcohol dependence works better in individuals who possess specific combinations of genes that regulate the function and binding of serotonin, a brain chemical affected by the treatment, according to a study supported by the National Institutes of Health. A report of the finding appears online in the American Journal of Psychiatry.
Using advanced analysis of DNA from Y chromosomes from men all over the world, scientists have shed new light on the mystery of when and how a few early human ancestors started to give rise to the incredible diversity of today’s population.
Researchers at UCLA’s Jonsson Comprehensive Cancer Center have successfully combined cellular therapy and gene therapy in a mouse model system to develop a viable treatment strategy for breast cancer that has metastasized to the patient’s brain.
Researchers at the University of California, San Diego School of Medicine report a simple, easily reproducible RNA-based method of generating human induced pluripotent stem cells (iPSCs) in the August 1 edition of Cell Stem Cell. Their approach has broad applicability for the successful production of iPSCs for use in human stem cell studies and eventual cell therapies.
A good state of mind — that is, your happiness — affects your genes, say scientists from UCLA's Cousins Center for Psychoneuroimmunology and the University of North Carolina. They examined how positive psychology impacts human gene expression and found that different types of happiness have surprisingly different effects on the human genome.
Now a special issue of the journal CHAOS, produced by AIP Publishing, explores new experimental and theoretical techniques for unraveling genetic networks.
Scientists have identified new genetic mutations that can cause pulmonary arterial hypertension (PAH), a rare fatal disease characterized by high blood pressure in the lungs. The mutations, found in the gene KCNK3, appear to affect potassium channels in the pulmonary artery, a mechanism not previously linked to the condition. Cell culture studies showed that the mutations’ effects could be reversed with a drug compound known as a phospholipase inhibitor. The study was published today in the online edition of the New England Journal of Medicine.
A researcher from the Perelman School of Medicine at the University of Pennsylvania and colleagues have identified the genetic mutation in Africans with HIV that puts them at a much higher risk for tuberculosis infections.
The resistance to insulin seen in type 2 diabetics is caused partly by the lack of a protein that has not previously been associated with diabetes. This breakthrough could potentially help to prevent diabetes.
Painstaking new analysis of the genetic sequence of the X chromosome—long perceived as the “female” counterpart to the male-associated Y chromosome—reveals that large portions of the X have evolved to play a specialized role in sperm production.
In Nature this week, Santa Fe Institute External Professor Andreas Wagner and University of Zurich colleague Aditya Barve, by simulating changes in an organism’s metabolism, show that most traits may emerge as non-crucial "exaptations" rather than as selection-advantageous adaptations.
Several companies sell genetic testing directly to consumers, but little research has been done on how consumers experience such tests. Now, a study is providing insight into how a diverse sample of primary care patients experience genetic testing.
Scientists at the National Cancer Institute (NCI) have generated a data set of cancer-specific genetic variations and are making these data available to the research community, according to a study published in Cancer Research, a journal of the American Association for Cancer Research.
A set of proteins involved in the body’s natural defenses produces a large number of mutations in human DNA, according to a study led by researchers at the National Institutes of Health. The findings suggest that these naturally produced mutations are just as powerful as known cancer-causing agents in producing tumors.
A Johns Hopkins study finds that healthy people who carry a genetic mutation for arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) are at much higher risk of developing the symptoms of the life-threatening heart disease if they participate in endurance sports and frequent exercise. The study also suggests that those carriers who significantly cut back on their exercise regimen may reduce their risk or delay the onset of symptoms.