A new study from researchers at the University of Michigan Comprehensive Cancer Center found that a subset of immune cells provide a niche where cancer stem cells survive.
By investigating regeneration in planarian flatworms, Whitehead Institute researchers have identified a mechanism—involving the interplay of two wound-induced genes—by which the animal can distinguish between wounds that require regeneration and those that do not.
Ground-breaking new research from a team of evolutionary biologists at Indiana University shows for the first time how asexual lineages of a species are doomed not necessarily from a long, slow accumulation of new mutations, but rather from fast-paced gene conversion processes that simply unmask pre-existing deleterious recessive mutations.
Cell senescence, an irreversible arrest of proliferation, is thought to be associated with normal aging and is protective against cancer. Penn researchers found that senescent cells undergo changes in their chromatin, similar to changes in cells that are prematurely aging. When the nuclear protein lamin B1 is deleted in senescent cells, large-scale changes in gene expression occurred. This loss of lamin B1 may cause changes in chromatin architecture and add to premature cell aging.
Problems with a key group of enzymes called topoisomerases can have profound effects on the genetic machinery behind brain development and potentially lead to autism spectrum disorder (ASD), according to research announced today in the journal Nature. Scientists at the University of North Carolina School of Medicine have described a finding that represents a significant advance in the hunt for environmental factors behind autism and lends new insights into the disorder’s genetic causes.
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.
Like volunteers handing out cups of energy drinks to marathon runners, specially engineered “helper cells” transplanted along with stem cells can dole out growth factors to increase the stem cells’ endurance, at least briefly, Johns Hopkins researchers report. Their study, published in the September issue of Experimental Neurology, is believed to be the first to test the helper-cell tactic, which they hope will someday help to overcome a major barrier to successful stem cell transplants.
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.
Researchers from the Perelman School of Medicine at the University of Pennsylvania demonstrate for the first time that the immune system influences the skin microbiome. A new study found that the skin microbiome – a collection of microorganisms inhabiting the human body – is governed, at least in part, by an ancient branch of the immune system called complement.
The technology that peeks underneath clothing at airport security screening check points has great potential for looking underneath human skin to diagnose cancer at its earliest and most treatable stages, a scientist said here today. The report on efforts to use terahertz radiation – “T-rays” – in early diagnosis of skin cancer was part of the 246th National Meeting & Exposition of the American Chemical Society, the world’s largest scientific society.
Glimpses of the nursery of life on Earth more than 3.5 billion years ago are coming from an unlikely venue almost 1 billion miles away, according to the leader of an effort to understand Titan, one of the most unusual moons in the solar system. In the talk here today at the 246th National Meeting & Exposition of the American Chemical Society, he said that Titan is providing insights into the evolution of life.
Jan-Michael Peters and his team at the Research Institute of Molecular Pathology (IMP) found that the structure of Chromosomes is supported by a kind of molecular skeleton, made of cohesin. Their discovery is published in the current online-issue of the journal NATURE.
Researchers at Johns Hopkins and elsewhere have brought new clarity to the picture of what goes awry in the brain during Parkinson’s disease and identified a compound that eases the disease’s symptoms in mice. Their discoveries, described in a paper published online in Nature Neuroscience on August 25, also overturn established ideas about the role of a protein considered key to the disease’s progress.
New research led by scientists at The University of Texas Health Science Center at Houston (UTHealth) and Baylor College of Medicine could aid efforts to diagnose and treat one of the most lethal and hard-to-treat types of cancer.
By carefully adjusting the function of crucial immune cells called Tregs, scientists may have developed a completely new type of cancer immunotherapy—harnessing the body’s immune system to attack tumors.
Man, a mouse or a microbe, stress is bad. Experiments in bacteria by molecular biologists have uncovered the mechanism that translates stress, such as exposure to extreme temperature, into temporarily blocked cell growth. Bacteria deal with stress by destroying proteins needed for replication.
Scientists at The Scripps Research Institute have discovered the molecular mechanism by which the deadly Ebola virus assembles, providing potential new drug targets. Surprisingly, the study showed that the same molecule that assembles and releases new viruses also rearranges itself into different shapes, with each shape controlling a different step of the virus’s life cycle.
By studying the planarian flatworm, a master of regenerating missing tissue and repairing wounds, the lab of Whitehead Institute Member Peter Reddien has identified an unexpected source of position instruction: the muscle cells in the planarian body wall. This is the first time that such a positional control system has been identified in adult regenerative animals.
Sympathetic neurons “cross-talk” -- or engage in reciprocal signaling -- with the tissues they connect to. And when they don't, there's trouble.
In a paper published in the Journal of Cell Biology, Sharon Campbell, PhD, professor of Biochemistry and Biophysics and member of UNC Lineberger Comprehensive Cancer Center, and Clare Waterman of the National Heart, Lung and Blood Institute at the National Institutes of Health showed that cell mobility occurs through the interactions between the protein vinculin and the cytoskeletal lattice formed by the protein actin. By physically binding to the actin that makes up the cytoskeleton, vinculin operates as a form of molecular clutch transferring force and controlling cell motion.
When egg and sperm combine, the new embryo bustles with activity. Its cells multiply so rapidly they largely ignore their DNA, other than to copy it and to read just a few essential genes. The embryonic cells mainly rely on molecular instructions placed in the egg by its mother in the form of RNA.
A little-studied factor known as the Little Elongation Complex (LEC) plays a critical and previously unknown role in the transcription of small nuclear RNAs (snRNA), according to a new study led by scientists at the Stowers Institute for Medical Research and published in the Aug. 22, 2013, issue of the journal Molecular Cell.
Scientists at Sanford-Burnham Medical Research Institute have identified a key factor that regulates the autophagy process, a kind of cleansing mechanism for cells in which waste material and cellular debris is gobbled up to protect cells from damage, and in turn, modulates aging.
Proteins are the workhorses of cells, adopting conformations that allow them to set off chemical reactions, send signals and transport materials. But when a scientist is designing a new drug, trying to visualize the processes inside cells, or probe how molecules interact with each other, they can't always find a protein that will do the job they want. Instead, they often engineer their own novel proteins to use in experiments, either from scratch or by altering existing molecules.
Researchers from Case Western Reserve University School of Medicine and the Dana-Farber Cancer Institute have discovered a new molecular pathway responsible for causing heart failure and showed that a first-in-class prototype drug, JQ1, blocks this pathway to protect the heart from damage.
Researchers at Sanford-Burnham Medical Research Institute now have a more complete picture of one particular pathway that can lead to cancer and diabetes. In the study published by Molecular Cell, the scientists uncovered how a protein called p62 has a cascade affect in regulating cell growth in response to the presence of nutrients such as amino acids and glucose.
Study findings describe an entirely new approach to enhance normal tissue growth, a discovery that could lead to advances in organ regeneration and help patients with a wide variety of medical conditions.
More than 11,000 Americans suffer spinal cord injuries each year, and since over a quarter of those injuries are due to falls, the number is likely to rise as the population ages. The reason so many of those injuries are permanently disabling is that the human body lacks the capacity to regenerate nerve fibers. The best our bodies can do is route the surviving tissue around the injury site.
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 University of Iowa-led team has found a promising, new way to treat asthma: Target an enzyme in airway lining cells. The finding could lead to the development of drugs that block the enzyme, CaMKII, from excessive oxidation, which can trigger asthma attacks.
Biologists at The Scripps Research Institute have made a significant discovery that could lead to a new therapeutic strategy for Parkinson’s disease. The findings focus on an enzyme known as parkin, whose absence causes an early-onset form of Parkinson’s disease.
Key molecular pathways that lead to late-onset Alzheimer's disease have been identified by neuroscientists at Columbia University Medical Center. Published in Nature, findings present a new approach to Alzheimer’s research and highlight several new potential drug targets.
The pulmonary vasculature, the blood vessels that connect the heart to the lung, develops even in the absence of the lung. Mice in which lung development is inhibited still have pulmonary blood vessels, which revealed to the researchers that cardiac progenitors, or stem cells, are essential for cardiopulmonary co-development.
A rapid and highly efficient system for transferring large molecules, nanoparticles, and other agents into living cells opens new avenues for disease research and treatment.
Stowers investigators use genetics and live cell imaging to illuminate molecular mechanisms that position the cell division machinery in growing tissues.
Protein production or translation is tightly coupled to a highly conserved stress response—the heat shock response and its primary regulator, heat shock factor 1 (HSF1)—that cancer cells rely on for survival and proliferation, according to Whitehead Institute researchers. In mouse models of cancer, therapeutic inhibition of translation interrupts HSF1’s activity, dramatically slowing tumor growth and potentially rendering drug-resistant tumors responsive to other therapies.
For more than 125 years, scientists have been peering through microscopes, carefully watching cells divide. Until now, however, none has actually seen how cells manage to divide precisely into two equally-sized daughter cells during mitosis. Such perfect division depends on the position of the mitotic spindle (chromosomes, microtubules, and spindle poles) within the cell, and it’s now clear that human cells employ two specific mechanisms during the portion of division known as anaphase to correct mitotic spindle positioning.
A team of researchers from Case Western Reserve University School of Medicine have identified a mechanism that can prevent the normal prion protein from changing its molecular shape into the abnormal form responsible for neurodegenerative diseases.
Researchers have identified a self-perpetuating signaling circuit inside connective tissue cells that allows these cells to propel themselves in a particular direction, just as tumor cells do when invading healthy tissue during cancer metastasis.
The protein TAp73 is a relative of the well-known, tumor-suppressor protein p53, yet it is still not known whether TAp73 enhances tumor cell growth and, if so, exactly how. Penn researchers found that TAp73 supports the proliferation of human and mouse tumor cells. They also identify an important mechanism by which TAp73 gives tumor cells a growth advantage: it activates the expression of an enzyme important for cell replications and anti-oxidant protection.
New Department of Systems Biology at Columbia University Medical Center is developing a different approach to cancer clinical trials, in which therapies are designed and tested one patient at a time. The patient’s tumor is “reverse engineered” to determine its unique genetic characteristics and to identify existing U.S. Food and Drug Administration (FDA)-approved drugs that may target them.
Scientists have captured new details of the biochemical interactions necessary for cell division. The research may suggest ways for stopping cell division when it goes awry.
Salk researchers' findings on chromosome shortening suggest a potential target to arrest cancer cell growth.
Chemists from North Carolina State University have performed a DNA-based logic-gate operation within a human cell. The research may pave the way to more complicated computations in live cells, as well as new methods of disease detection and treatment.
Findings of disrupted micronuclei may prove to be a valuable tool for detecting cancer.
A mere 25 years ago, noncoding RNAs were considered nothing more than "background noise." Now two new studies by researchers at Beth Israel Deaconess Medical Center reveals that miR-22 plays an outsized role in cancer.
Lake Vostok, buried under a glacier in Antarctica, is so dark, deep and cold that scientists had considered it a possible model for other planets, a place where nothing could live. However, work by Dr. Scott Rogers, a Bowling Green State University professor of biological sciences, and his colleagues has revealed a surprising variety of life forms living and reproducing in this most extreme of environments.
A research team has genetically engineered a mouse with glowing primary cilia, the tiny outgrowths seen on the surface of most cells, according to a study published today in BioMed Central’s open access journal, Cilia.
Johns Hopkins cancer scientists have discovered that a little-described gene known as FAM190A plays a subtle but critical role in regulating the normal cell division process known as mitosis, and the scientists’ research suggests that mutations in the gene may contribute to commonly found chromosomal instability in cancer.
University of Chicago researchers have discovered the first human "bifunctional" gene--a single gene that creates a single mRNA transcript that codes for two different proteins, simultaneously. Their finding elucidates a previously unknown mechanism in our basic biology, and has potential to guide therapy for at least one neurological disease.
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