Whitehead Institute scientists have for the first time identified a protein that appears to be a nutrient sensor for the key growth-regulating mTORC1 metabolic pathway.
Enzymes linked to diabetes and obesity appear to play key roles in arthritis and leukemia, potentially opening up new avenues for treating these diverse diseases, according to researchers at Washington University School of Medicine in St. Louis.
For a skin cell to do its job, it must turn on a completely different set of genes than a liver cell — and keep genes it doesn’t need switched off. One way of turning off large groups of genes at once is to send them to “time-out” at the edge of the nucleus. New research shows how DNA gets sent to the nucleus’ far edge, a process critical to controlling genes and determining cell fate.
New work shows that bacteria (and probably other cells as well) don’t double in mass before dividing. Instead they add a constant volume (or mass) no matter what their initial size. A small cell adds the same volume as a large cell. By following this rule a cell population quickly converges on a common size.
UCLA researchers have for the first time developed a method that defines many stages of reprogramming skin or blood cells into pluripotent stem cells. Study analyzed the reprogramming process at the single-cell level on a daily basis. Results determined that stages of cell change were the same across different reprogramming systems and cell types analyzed.
When University of Utah biologists fed mice sugar in doses proportional to what many people eat, the fructose-glucose mixture found in high-fructose corn syrup was more toxic than sucrose or table sugar, reducing both the reproduction and lifespan of female rodents.
When it comes to skin infections, a healthy and robust immune response may depend greatly upon what lies beneath. In a new paper published in the January 2, 2015 issue of Science, researchers at the University of California, San Diego School of Medicine report the surprising discovery that fat cells below the skin help protect us from bacteria.
Results from a study published on Jan. 2 in Science defy textbook science, showing for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints – DNA and an intermediate template called messenger RNA (mRNA). A team of researchers has observed a case in which another protein specifies which amino acids are added.
Scientists from the Johns Hopkins Kimmel Cancer Center have created a statistical model that measures the proportion of cancer incidence, across many tissue types, caused mainly by random mutations that occur when stem cells divide. By their measure, two-thirds of adult cancer incidence across tissues can be explained primarily by “bad luck,” when these random mutations occur in genes that can drive cancer growth, while the remaining third are due to environmental factors and inherited genes.
Already known to cut proteins, the enzyme SPPL3 turns out to have additional talents, according to a new study from Johns Hopkins. In its newly discovered role, SPPL3 works without cutting proteins to activate T cells, the immune system’s foot soldiers. Because its structure is similar to that of presenilin enzymes, which have been implicated in Alzheimer’s disease, the researchers believe their findings could shed more light on presenilin functions, in addition to providing new insight into how the immune system is controlled.
Researchers at Johns Hopkins have discovered what keeps an enzyme from becoming overzealous in its clipping of DNA. Since controlled clipping is required for the production of specialized immune system proteins, an understanding of what keeps the enzyme in check should help explain why its mutant forms can lead to immunodeficiency and cancer.
Vanderbilt mathematician Glenn Webb and NYU microbiologist Martin Blaser propose that the microbes which live on our bodies may have influenced the age structure of human populations in prehistoric times.
New research from The Johns Hopkins University suggests that the amount of mitochondrial DNA (mtDNA) found in peoples’ blood directly relates to how frail they are medically. This DNA may prove to be a useful predictor of overall risk of frailty and death from any cause 10 to 15 years before symptoms appear.
UT Southwestern Medical Center neurology researchers have identified an important cell signaling mechanism that plays an important role in brain cancer and may provide a new therapeutic target.
Known as the “inside-out” theory of eukaryotic cell evolution, an alternative view of how complex life came to be was published recently in the open access journal BMC Biology.
Dave Pagliarini, a UW-Madison assistant professor of biochemistry, recently published two studies shedding more light on coenzyme Q and how it’s made, one in the Proceedings of the National Academy of Science (PNAS) in October and another today in Molecular Cell.
Near-perfect replications of human and animal cells enables improved study of certain cancers and stem cells, as well as the creation of complex durable objects without machinery.
Long known for its ability to help organisms successfully adapt to environmentally stressful conditions, the highly conserved molecular chaperone heat-shock protein 90 (HSP90) also enables estrogen receptor-positive (ER+) breast cancers to develop resistance to hormonal therapy.
Three “Tell Your Own Cell Story” videos commissioned by Celldance Studios, a.k.a. the ASCB’s Public Information Committee premiere online from the 2014 ASCB/IFCB meeting in Philadelphia on Monday, December 8. All three are streamable and downloadable. www.ascb.org/celldance-2014
In work to be presented at the ASCB/IFCB meeting in Philadelphia, researchers from the Institut Curie in Paris report that they have evidence of a coordinated attack on the basement membrane of human colon cells by cancer cells in situ and CAF cells in the extracellular matrix that begins long before the actual translocation of cancer cells.
Now bioengineering researchers at Temple University in Philadelphia have come up with an experimental workaround—a synthetic pediatric blood-brain barrier on a small chip—and have tested it successfully using rat brain endothelial cells (RBECs) from rat pups and human endothelial cells.
Jae-Won Shin and David Mooney of Harvard University’s Wyss Institute for Biologically Inspired Engineering in Cambridge, MA, describe building a three-dimensional (3D) hydrogel system with tunable stiffness to see how relative stiffness of the surrounding ECM affected the resistance of human myeloid leukemias to chemotherapeutic drugs.
The even more surprising answer was that rescuing the Golgi reduced Aβ accumulation significantly, apparently by re-opening a normal protein degradation pathway for the amyloid precursor protein (APP).
The average animal cell is 10 microns across but why? Princeton bioengineers take their story of gravity in cells one step further at ASCB, describing how cells manage to support thousands of membrane-less compartments inside the nucleus
A new method uses photoactivatable complementary fluorescent proteins (PACF) to observe and quantify protein-protein interactions in live cells at the single molecule level.
The search for a living laboratory model of Alzheimer’s disease (AD)—the so-called “Alzheimer’s in a dish”—has a new candidate. Håkan Toresson and colleagues at Lund University in Sweden report success in creating induced neurons that model Alzheimer’s by starting with fibroblasts taken from skin biopsies.
“This new research tool offers us a more profound view of the immune responses that are involved in a range of diseases, such as HIV infection. At the level of gene transcription, this had been difficult, complex and costly to do with current technologies, such as microscopy” - Dr. Daniel Kaufmann, University of Montreal Hospital Research Centre
Researchers at the Mechanobiology Institute at the National University of Singapore have comprehensively described the network of proteins involved in cell-cell adhesions, or the cadherin interactome. This work was published in Science Signaling (Guo et al. E-cadherin interactome complexity and robustness resolved by quantitative proteomics, Science Signaling, 02 Dec 2014, Vol 7, Issue 354).
Salk researchers tinker with a time-restricted diet in mice and find that it is remarkably forgiving.
Replenishing the supply of a molecule that normally activates cannabinoid receptors in the brain could relieve mood and anxiety disorders and enable some people to quit using marijuana, a Vanderbilt University study suggest
Researchers can now explore viruses, bacteria and components of the human body in more detail than ever before with software developed at The Scripps Research Institute. In a study published December 1 in the journal Nature Methods, the researchers demonstrated how the software, called cellPACK, can be used to model viruses such as HIV.
Scientists have believed that the lengthening of those repeats occur during DNA replication when cells divide or when the cellular DNA repair machinery gets activated. Recently, however, Tufts University researchers have traced expansive repeats to the process called transcription, which is copying the information from DNA into RNA.
Using a new imaging technique, National Institutes of Health researchers have found that the biological machinery that builds DNA can insert molecules into the DNA strand that are damaged as a result of environmental exposures. These damaged molecules trigger cell death that produces some human diseases, according to the researchers. The work, appearing online Nov. 17 in the journal Nature, provides a possible explanation for how one type of DNA damage may lead to cancer, diabetes, hypertension, cardiovascular and lung disease, and Alzheimer’s disease.
A team led by scientists from The Scripps Research Institute has found a simple method to convert human skin cells into the specialized neurons that detect pain, itch, touch and other bodily sensations and are affected by spinal cord injury and involved in Friedreich’s ataxia.
A multi-disciplinary research team from the National University of Singapore (NUS) has made a breakthrough discovery of a new type of immune cells that may help in the development of a future treatment for multiple sclerosis (MS).
Berkeley Lab scientists have learned new details about how an important tumor-suppressing protein, called p53, binds to the human genome. As with many things in life, they found that context makes a big difference.
Life's extremists, a family of microbes called Archaea, may be an untapped source of new antibacterial drugs. That conclusion arises from the discovery of the first antibacterial gene in this ancient lineage.
The cohesin molecule ensures the proper distribution of DNA during cell division. Scientists at the Research Institute of Molecular Pathology (IMP) in Vienna can now prove the concept of its carabiner-like function by visualizing for the first time the open form of the complex. The journal SCIENCE publishes the new findings in its current issue.
While investigating a rare genetic disorder, researchers at the University of California, San Diego School of Medicine have discovered that a ubiquitous signaling molecule is crucial to cellular reprogramming, a finding with significant implications for stem cell-based regenerative medicine, wound repair therapies and potential cancer treatments.
The new method lets researchers identify weak and previously undetectable interactions between proteins inside living cells
Underlying circadian rhythms is a clock built of transcription factors that control the oscillation of genes, serving as the wheels and springs of the clock. But, how does a single clock keep time in multiple phases at once? A genome-wide survey found that circadian genes and regulatory elements called enhancers oscillate daily in phase with nearby genes – both the enhancer and gene activity peak at the same time each day.
Researchers debate whether the lung tissue in pulmonary fibrosis is directly damaged, or whether immune cells initiate the scarring process – an important distinction when trying to find new ways to battle the disease. Now research shows that both processes may be important, and suggest a new direction for developing novel therapies.
Case Western Reserve researchers have identified a protein mutation that alters specific gender-related tissue in males before birth and can contribute to cancer and other less life-threatening challenges. The findings appear in the November 21 edition of the Journal of Biological Chemistry.
Protein misfolding” diseases such as cystic fibrosis and Alzheimer’s may be seriously exacerbated by the body’s own response against that misfolding, according to a new study led by scientists at The Scripps Research Institute.
Dr. Maya Schuldiner’s lab has identified an unusual cellular mechanism – a two-part zinc pump – that is faulty in some types of Alzheimer’s. While it’s not yet clear how the finding links to Alzheimer’s, it does offer new directions for investigating the causes of the disease.
An anti-cancer drug protects normal cells from radiation damage and increases the effectiveness of radiation therapy in prostate cancer models
New research in flies shows how cells in adult reproductive organs maintain their sexual identity. The study, published online on Nov. 13 in Developmental Cell, also identified a mutation that can switch the cells’ sexual identity. The findings could lead to new insights on how to alter cells for therapeutic purposes.
A team from the Morgridge Institute for Research regenerative biology group, led by University of Wisconsin-Madison professor and stem cell pioneer James Thomson, discovered a way to impose an immortal-like state on mouse progenitor cells responsible for producing blood and vascular tissue. By regulating a small number of genes, the cells became “trapped” in a self-renewing state and capable of producing functional endothelial, blood and smooth muscle cells.
Scientists have mostly ignored mRNA, the molecule that ferries information from DNA to the cellular machines that make proteins, because these DNA transcripts are ephemeral and soon destroyed. But mRNA can be just as important as DNA scientists at Washington University in St. Louis say. They found that oxidized messenger RNA jams the cellular machines that make protein. The failure to clear the jams and chew up bad messengers is associated with neurodegenerative diseases such as Alzheimer’s.
Molecules called long non-coding RNAs (lncRNAs) have been implicated in breast cancer but exactly why they cause metastasis and tumor growth has been little understood…until now.
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