The same trait that makes a rare immune cell invaluable in fighting some infections also can be exploited by other diseases to cause harm, two new studies show.
The delivery system for an important class of proteins in the cell membrane can be fully replicated with a mere three components, according to a new study published in Nature.
Researchers at the Joslin Diabetes Center have shown that an enzyme found in the mitochondria of cells is decreased in the skeletal muscle of those with type 2 diabetes, a finding that could lead to the development of drugs to boost the activity of this enzyme in an effort to fight the disease.
Researchers at NYU School of Medicine have discovered the cellular mechanisms that normally generate chromosomal breaks in bacteria such as E. coli. The study’s findings are published in the August 18 issue of the journal Cell.
New findings by scientists at the Broad Institute of MIT and Harvard and Whitehead Institute point to a decentralized society in tumors, with cancer cells able to interconvert between different types. These results have potential implications for the treatment of tumors, in particular, that attacking cancer stem cells alone may not be enough to fight cancer.
A visiting researcher from Sweden in the Indiana University College of Arts and Sciences' Biology Department has led an international team in culturing, characterizing and formally naming a new class of fungi that previously had only been identified through DNA sequencing from environmental samples.
Stem cell researchers at UCLA have discovered that three types of cells derived from human embryonic stem cells and induced pluripotent stem cells are similar to each other, but are much more developmentally immature than previously thought when compared to those same cell types taken directly from human tissue.
Researchers at the Johns Hopkins University School of Medicine have found a protein normally involved in blood pressure regulation in a surprising place: tucked within the little “power plants” of cells, the mitochondria. The quantity of this protein appears to decrease with age, but treating older mice with the blood pressure medication losartan can increase protein numbers to youthful levels, decreasing both blood pressure and cellular energy usage. The researchers say these findings, published online during the week of August 15, 2011, in the Proceedings of the National Academy of Sciences, may lead to new treatments for mitochondrial–specific, age-related diseases, such as diabetes, hearing loss, frailty and Parkinson’s disease.
A research team led by St. Jude Children’s Research Hospital scientists has identified a potential new target for treatment of the childhood eye tumor retinoblastoma. Their work also settles a scientific debate by showing the cancer’s cellular origins are as scrambled as the developmental pathways at work in the tumor.
In a new study published in the August 16th issue of Developmental Cell, researchers at NYU Langone Medical Center identified a molecular mechanism that guarantees that new blood vessels form in the right place and with the proper abundance.
Salmonella cells have hijacked the protein-building process to maintain their ability to cause illness, new research suggests.
New research led by Derya Unutmaz, MD associate professor, the Departments of Pathology, Medicine, and Microbiology at NYU School of Medicine and Mark Sundrud, PhD, of Tempero Pharmaceuticals, Inc., has identified a novel sensory pathway that modulates the potency of Th17 cell responses. The new research is highlighted in the August 8th online edition of the Journal of Experimental Medicine.
UVA Health System researchers have made a pivotal discovery in understanding the complicated process of neurogenesis, and their findings could one day help scientists devise novel therapies to promote neurogenesis in the adult brain and re-establish its function in patients suffering from depression, post-traumatic stress disorder, and other mental disorders, in which adult neurogenesis is impaired.
Our bodies are perfectly capable of renewing billions of cells every day but fail miserably when it comes to replacing damaged organs such as kidneys. Using the flatworm Schmidtea mediterranea—famous for its capacity to regrow complete animals from minuscule flecks of tissue—as an eloquent example, researchers at the Stowers Institute for Medical Research demonstrated how our distant evolutionary cousins regenerate their excretory systems from scratch.
Stem cell researchers at UCLA have uncovered for the first time why adult human cardiac myocytes have lost their ability to proliferate, perhaps explaining why the human heart has little regenerative capacity.
A person’s ability to battle viruses at the cellular level remarkably resembles the way deadly infectious agents called prions misfold and cluster native proteins to cause disease, UT Southwestern Medical Center researchers report.
New findings from the Monell Center may lend insight into why some people are especially sensitive to bitter tastes. Researchers have identified a protein inside of taste cells that acts to shorten bitter taste signals. Mice lacking the gene for this taste terminator protein are more sensitive to bitter taste and also find it more aversive.
The ability to tag proteins with a green fluorescent light to watch how they behave inside cells so revolutionized the understanding of protein biology that it earned the scientific teams who developed the technique Nobel Prizes in 2008. Now, researchers at Weill Cornell Medical College have developed a similar fluorescent tool that can track the mysterious workings of the various forms of cellular RNA.
The eon-spanning clock of evolution – the millions of years that generally pass before organisms acquire new traits – belies a constant ferment in the chambers and channels of cells, as changes in genes and proteins have subtle ripple effects throughout an organism. In a study in the July 29 issue of Science, scientists at Dana-Farber Cancer Institute’s Center for Cancer Systems Biology and an international team of colleagues capture the first evidence of the evolutionary process within networks of plant proteins.
Salk Institute and Dana Farber Cancer Institute researchers contribute to production of largest-ever map of plant protein interactions.
Using a “systems biology” approach – which focuses on understanding the complex relationships between biological systems – to look under the hood of an aggressive form of breast cancer, researchers for the first time have identified a set of proteins in the blood that change in abundance long before the cancer is clinically detectable.
Cells that were thought to be identical and responsible both for setting the body’s circadian rhythm and for the pupil’s reaction to light and darkness, are actually two different cells, each responsible for one of those tasks.
An approach developed at the Weizmann Institute could make adoptive cell transfer cancer therapy cheaper and more effective.
A regulatory T cell that expresses three specific genes shuts down the mass production of antibodies launched by the immune system to attack invaders, a team led by scientists at The University of Texas MD Anderson Cancer Center reported online in the journal Nature Medicine.
A molecular technique originally developed at the University of North Carolina at Chapel Hill has taken one step closer to becoming a treatment for the devastating genetic disease Duchenne muscular dystrophy.
The discovery of the mechanism of action behind a novel class of anticancer drugs designed to disrupt cancer cell mitochondrial metabolism may be a major step toward furthering clinical trials of the agents.
Scientists have identified a family of proteins that close a critical gap in an enzyme that is essential to all life, allowing the enzyme to maintain its grip on DNA and start the activation of genes. The enzyme, called RNA polymerase, is responsible for setting gene expression in motion in all cells.
A simple cut to the skin unleashes a complex cascade of chemistry to stem the flow of blood. Now, scientists at Washington University School of Medicine in St. Louis have used evolutionary clues to reveal how a key clotting protein assembles. The finding sheds new light on common bleeding disorders.
Drug developers have long been looking for agents that will target a cell receptor that regulates stress in humans, but no small molecule drugs have successfully gone through clinical studies. Now, a team at the Salk Institute has demonstrated how a novel tool can be used to map the binding sites on this receptor, which they say could speed the design of effective therapies.
A new study describes how hyperactivation of AMP-activated protein kinase (AMPK) promotes neurodegeneration in Huntington’s disease (HD). The article appears online on July 18, 2011, in The Journal of Cell Biology.
Novel contrast agents that sneak into bacteria disguised as glucose food can detect bacterial infections in animals with high sensitivity and specificity. These agents -- called maltodextrin-based imaging probes -- can also distinguish a bacterial infection from other inflammatory conditions.
St. Jude Children’s Research Hospital scientists have identified a key immune system regulator, a protein that serves as a gatekeeper in the white blood cells that produce the “troops” to battle specific infections.
Using two methods, Whitehead researchers have manipulated targeted genes in both human embryonic stem (ES) cells and induced pluripotent stem (iPS) cells. In one case, scientists employed proteins known as ZFNs to change a single base pair in the genome, allowing them either to insert or remove mutations known to cause early-onset Parkinson’s disease (PD).
Stowers researchers pinpoint the Super Elongation Complex as a major regulator in the coordinated expression of early developmental genes.
Successful gene expression requires the concerted action of a host of regulatory factors. Long overshadowed by bonafide transcription factors, coactivators—the hanger-ons that facilitate transcription by docking onto transcription factors or modifying chromatin—have recently come to the fore.
Farmers and other astute observers of nature have long known that crops like corn and sorghum grow taller at night. But the biochemical mechanisms that control this nightly stem elongation, common to most plants, have been something of a mystery to biologists—until now.
A small protein called SUMO might prevent the protein aggregations that typify Parkinson’s disease (PD), according to a new study in the July 11, 2011, issue of The Journal of Cell Biology.
Oh, the challenges of being a neuron, responsible for essential things like muscle contraction, gland secretion and sensitivity to touch, sound and light, yet constantly bombarded with signals from here, there and everywhere.
A discovery by University of Alabama at Birmingham researchers about a how a common cell pathway that helps regulate cell survival and production is turned on could lead to new treatments for autoimmune diseases and cancer.
Researchers at the Salk Institute have been able to genetically incorporate "unnatural" amino acids, such as those emitting green fluorescence, into neural stem cells, which then differentiate into brain neurons with the incandescent "tag" intact.
This study showed that pluripotent cells are not all equal. The researchers discovered the fate – or destination – of human pluripotent stem cells is encoded by how their DNA is arranged, and this can be detected by specific proteins on the surface of the stem cells.
A report from the Conaway lab at the Stowers Institute for Medical Research in the July 8, 2011, edition of the journal Cell identifies a switch that allows RNA polymerase to shift gears from neutral into drive and start transcribing. This work sheds light on a process fundamental to all plant or animal cells and suggests how transcriptional anomalies could give rise to tumors.
By mapping various genomes onto an X-Y axis, a team comprised mostly of Kansas State University researchers has found that Charles Darwin and a fruit fly -- among other organisms -- have a lot in common genetically.
Excess nutrients, such as fat and sugar, don’t just pack on the pounds but can push some cells in the body over the brink. Unable to tolerate this “toxic” environment, these cells commit suicide. Now, scientists at Washington University School of Medicine in St. Louis have discovered three unexpected players that help a cell overloaded with fat initiate its own demise.
When researchers at the Buck Institute dialed back activity of a specific mRNA translation factor in adult nematode worms they saw an unexpected genome-wide response that effectively increased activity in specific stress response genes that could help explain why the worms lived 40 percent longer under this condition. The study highlights the importance of mRNA translation in the aging process.
Using ovarian surface epithelial cells from mice, researchers from Virginia Tech have released findings from a study that they believe will help in cancer risk assessment, cancer diagnosis, and treatment efficiency in a technical journal.
Molecular and cell biologists at the University of Virginia Health System have discovered new information about how the Ebola virus works that could eventually lead to new drug treatments for the deadly virus.
A Case Western Reserve University researcher has found that the environment not only weeds out harmful and useless mutations through natural selection, but actually influences helpful mutations, which are passed to the next generation. He challenges peers to repeat the controversial findings.
A new U-M study bring us one step closer to developing treatments for issues associated with aging or chronic diseases in which cells lose their ability to maintain a stable pattern of gene expression.
Scientists at the Salk Institute for Biological Studies have found clues to the functioning of an important damage response protein in cells. The protein, p53, can cause cells to stop dividing or even to commit suicide when they show signs of DNA damage, and it is responsible for much of the tissue destruction that follows exposure to ionizing radiation or DNA-damaging drugs such as the ones commonly used for cancer therapy. The new finding shows that a short segment on p53 is needed to fine-tune the protein’s activity in blood-forming stem cells and their progeny after they incur DNA damage.
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