A simple technique uses silica to coat a living cell both inside and outside. The process forms a near-perfect replica of the cell's structure, down to the tiniest organelle. The resulting model, heated, creates nature-sculpted nanotools with components far stronger than when built out of flesh.
UT Southwestern Medical Center scientists have synthesized a peptide that shows potential for pharmaceutical development into agents for treating infections, neurodegenerative disorders, and cancer through an ability to induce a cell-recycling process called autophagy.
You might think you have nothing in common with mustard except hotdogs. Yet based on research in a plant from the mustard family, Salk scientists have discovered a possible explanation for how organisms, including humans, directly regulate chemical reactions that quickly adjust the growth of organs. These findings overturn conventional views of how different body parts coordinate their growth, shedding light on the development of more productive plants and new therapies for metabolic diseases.
Researchers at Johns Hopkins have devised a way to detect whether cells previously transplanted into a living animal are alive or dead, an innovation they say is likely to speed the development of cell replacement therapies for conditions such as liver failure and type 1 diabetes. As reported in the March issue of Nature Materials, the study used nanoscale pH sensors and magnetic resonance imaging (MRI) machines to tell if liver cells injected into mice survived over time.
A team of biologists from Indiana University and Brown University believes it has discovered the mechanism by which interacting mutations in mitochondrial and nuclear DNA produce an incompatible genotype that reduces reproductive fitness and delays development in fruit flies.
Research from Whitehead Institute shows that transcription at the active promoters of protein-coding genes commonly runs in opposite directions. This leads to coordinated production of both protein-coding messenger RNAs (mRNAs) and long noncoding RNAs (lncRNAs).
Researchers found a key determinant in the balance between two proteins, BRCA1 and 53BP1, in DNA repair machinery. Breast and ovarian cancer are associated with a breakdown in the repair systems involving these proteins.
A new book presents the in-depth story about the men and women who created a new science, modern cell biology.
A new breakthrough marks the first time anyone has been able to show the actual temperature distribution inside living cells. This work will be presented at the 57th Annual Meeting of the Biophysical Society (BPS), held Feb. 2-6, 2013, in Philadelphia, Pa.
Researchers have developed a new non-contact, non-invasive tool to measure the mechanical properties of cells at the sub-cell scale. Their work will be presented at the 57th Annual Meeting of the Biophysical Society (BPS), held Feb. 2-6, 2013, in Philadelphia, Pa.
In this week's Nature Methods, Salk researchers share a how-to secret for biologists: code for Amazon Cloud that significantly reduces the time necessary to process data-intensive microscopic images.
Genetic analysis by Stowers investigators has implications for a genetic disorder known as Hirschsprung Syndrome.
Researchers at the Cedars-Sinai Heart Institute, whose clinical trial results in 2012 demonstrated that stem cell therapy reduces scarring and regenerates healthy tissue after a heart attack, now have found that the stem cell technique boosts production of existing adult heart cells (cardiomyocytes) and spurs recruitment of existing stem cells that mature into heart cells. The findings, from a laboratory animal study, are published in EMBO Molecular Medicine online.
Just like a comic book super hero, you could say that the enzyme superoxide dismutase (SOD1) has a secret identity. Since its discovery in 1969, scientists believed SOD1’s only role was to protect living cells against damage from free radicals. Now, researchers at the Johns Hopkins Bloomberg School of Public Health have discovered that SOD1 protects cells by regulating cell energy and metabolism.
Beta blockers inhibit cancer progression, decrease mortality.
Ever since discovering a decade ago that a gene altered in lung cancer regulated an enzyme used in therapies against diabetes, Reuben Shaw has wondered if drugs originally designed to treat metabolic diseases could also work against cancer.
UCLA researchers, in a finding that runs counter to conventional wisdom, have discovered for the first time that a gene thought to express a protein in all cells that come under stress is instead expressed only in specific cell types.
Synapse development is promoted by a variety of cell adhesion molecules that connect neurons and organize synaptic proteins. Many of these adhesion molecules are linked to neurodevelopmental disorders; mutations in neuroligin and neurexin proteins, for example, are associated with autism and schizophrenia. According to a study in The Journal of Cell Biology, another family of proteins linked to these disorders regulates the function of neuroligins and neurexins in order to suppress the development of inhibitory synapses.
The spread of breast cancer to distant organs within the body, an event that often leads to death, appears in many cases to involve the loss of a key protein, according to UC San Francisco researchers, whose new discoveries point to possible targets for therapy.
Researchers at Moffitt Cancer Center and colleagues at Wayne State University School of Medicine investigated the acidity in solid tumors to determine if pH levels play a role in cancer cell invasion in surrounding tissues. They found that an acidic microenvironment can drive cancer cells to spread and propose that neutralizing pH would inhibit further invasion, providing a therapeutic opportunity to slow the progression of cancers.
Zhen Huang freely admits he was not interested in blood vessels four years ago when he was studying brain development in a fetal mouse. Instead, he wanted to see how changing a particular gene in brain cells called glia would affect the growth of neurons.
A University of North Carolina School of Medicine study may have implications for thwarting the effects of bio-terrorism attack with lethal microbes, as well as finding a way to save people in septic shock, an overwhelming bacterial infection of the blood.
After years of experimentation, researchers at the University of Arkansas have solved a complex, decades-old problem in membrane biochemistry.
For decades now, researchers have been trying, without success, to develop drugs that slow or prevent Alzheimer’s. Now research at UCLA suggests that while the protein they have been focusing on-- amyloid-beta—is the right one, what’s needed is to direct a drug to a very specific location, which they’ve discovered, on that protein.
The fight against triple-negative breast cancer takes three steps forward.
In lab tests, juice from rice cells knocked out two kinds of human cancer cells as well or better than the potent anti-cancer drug Taxol. Plus, it did something extra: it left normal cells unharmed.
A team of researchers based at Johns Hopkins has decoded a system that makes certain types of immune cells impervious to HIV infection. The system’s two vital components are high levels of a molecule that becomes embedded in viral DNA like a code written in invisible ink, and an enzyme that, when it reads the code, switches from repairing the DNA to chopping it up into unusable pieces.
New details emerge about a molecular surveillance system that helps detect and correct errors in mitosis that can lead to cell death or human diseases. Biologists can watch and record images of the key players including microtubules, kinetochores, molecular engines and the polar ejection force.
A research team led by the La Jolla Institute for Allergy & Immunology has discovered the mechanism that enables CD4 helper T cells to assume the more aggressive role of killer T cells in mounting an immune attack against viruses, cancerous tumors and other damaged or infected cells. The finding, made in collaboration with researchers from the RIKEN Institute in Japan, could enable the development of more potent drugs for AIDS, cancer and many other diseases based on using this mechanism to trigger larger armies of killer T cells against infected or damaged cells.
Scientists at the Research Institute of Molecular Pathology (IMP) in Vienna, Austria and at the University of Cologne, Germany have discovered the molecular basis underlying the patterned folding and assembly of muscle proteins. They describe the strikingly new mechanism in the current issue of Cell.
In a study published in the January 18 issue of Cell, researchers from the University of North Carolina Lineberger Comprehensive Cancer Center have developed a new method to visualize aging and tumor growth in mice using a gene closely linked to these processes.
In each cell, thousands of regulatory regions control which genes are active at any time. Scientists at the Institute of Molecular Pathology (IMP) in Vienna developed a method that reliably detects these regions and measures their activity. The new technology is published online by Science this week.
Researchers at the University of California, San Diego School of Medicine have identified a molecular mechanism regulating autophagy, a fundamental stress response used by cells to help ensure their survival in adverse conditions.
Researchers at the University of California, San Diego School of Medicine have discovered that hard-to-reach, drug-resistant leukemia stem cells (LSCs) that overexpress multiple pro-survival protein forms are sensitive – and thus vulnerable – to a novel cancer stem cell-targeting drug currently under development.
According to researchers at the Icahn School of Medicine at Mount Sinai, the flu knows how much time it has to multiply, infect other cells, and spread to another human being. If it leaves a cell too soon, the virus is too weak. If it leaves too late, the immune system has time to kill the virus.
Researchers characterized a new protein that affects how cells in the innate immune system function and protect humans against invading bacteria such as E. coli O157:H7.
Scientists at the UI and BYU have identified a gene that induces drug resistance in cancer. The finding could improve prognostic and diagnostic tools for evaluating cancer and monitoring response to treatment, and could lead to new therapies for eradicating drug-resistant cancer cells.
Researchers have identified a class of p53 target genes and regulatory molecules that represent more promising therapeutic candidates. p53 participates in a molecular feedback circuit with malic enzymes, thereby showing that p53 activity is also involved in regulating metabolism.
Scientists at the Texas Biomedical Research Institute in San Antonio have for the first time demonstrated that baboon embryonic stem cells can be programmed to completely restore a severely damaged artery. These early results show promise for eventually developing stem cell therapies to restore human tissues or organs damaged by age or disease.
Repression of a single protein in ordinary fibroblasts is sufficient to directly convert the cells – abundantly found in connective tissues – into functional neurons. The findings, which could have far-reaching implications for the development of new treatments for neurodegenerative diseases like Huntington’s, Parkinson’s and Alzheimer’s, will be published online in advance of the January 17 issue of the journal Cell.
Researchers have created a biophysical model of the response of a Gram-positive bacterium to the formation of a hole in its cell wall, then used experimental measurements to validate the theory.
Penn researchers have been studying the epigenetics enzyme HDAC3 for several years. They discovered that its activity requires interaction with a specific region on another protein called the Deacetylase Activating Domain. This “nuts and bolts” discovery on the epigenetic control of a person’s genome has implications for cancer and neurological treatments.
In an article published today in the journal Nature, an international research group describes how insulin binds to the cell to allow the cell to transform sugar into energy—and also how the insulin itself changes shape as a result of this connection.
Researchers at UCLA say it's not just what you eat that makes those pants tighter — it's also genetics. In a new study, scientists discovered that body-fat responses to a typical fast-food diet are determined in large part by genetic factors, and they have identified several genes they say may control those responses.
Research findings from the University of North Carolina School of Medicine are shining a light on an important regulatory role performed by the so-called dark matter, or “junk DNA,” within each of our genes.
Joslin Diabetes Center scientists have identified a cell cycle transcriptional co-regulator – TRIP-Br2 – that plays a major role in energy metabolism and fat storage. This finding has the potential to lead to new treatments for obesity.
In a novel use of gene knockout technology, researchers at the University of California, San Diego School of Medicine tested the same gene inserted into 90 different locations in a yeast chromosome – and discovered that while the inserted gene never altered its surrounding chromatin landscape, differences in that immediate landscape measurably affected gene activity.
Unlike less versatile muscle or nerve cells, embryonic stem cells are by definition equipped to assume any cellular role. Scientists call this flexibility “pluripotency,” meaning that as an organism develops, stem cells must be ready at a moment’s notice to activate highly diverse gene expression programs used to turn them into blood, brain, or kidney cells.
NYU biologists have identified how a vital protein is loaded by others into the centromere, the part of the chromosome that plays a significant role in cell division. Their findings shed new light on genome replication and may offer insights into the factors behind the production of abnormal numbers of chromosomes.
An international team, headed by researchers at the University of California, San Diego School of Medicine, has identified a key enzyme in the reprogramming process that promotes malignant stem cell cloning and the growth of chronic myeloid leukemia (CML), a cancer of the blood and marrow that experts say is increasing in prevalence.
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