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.
For the first time, scientists from the Florida campus of The Scripps Research Institute have identified small molecules that allow for complete control over a genetic defect responsible for the most common adult onset form of muscular dystrophy.
Research focused on the regulation of the adult stem cells that line the gastrointestinal tract of Drosophila suggests new models for the study of Barrett’s esophagus. Barrett’s esophagus is a condition in which the cells of the lower esophagus transform into stomach-like cells. In most cases this transformation has been thought to occur directly from chronic acid indigestion. A new study suggests a change in stem cell function for this transformation.
A team led by UC San Francisco researchers has discovered a sensory system in the foreleg of the fruit fly that tells male flies whether a potential mate is from a different species. The work addresses a central problem in evolution that is poorly understood: how animals of one species know not to mate with animals of other species.
A new study in PLOS ONE that examined food poisoning infection as-it-happens in mice revealed harmful bacteria, such as a common type of Salmonella, takes over beneficial bacteria within the gut amid previously unseen changes to the gut environment. The results provide new insights into the course of infection and could lead to better prevention or new treatments.
Using biochemistry and mass spectrometry, researchers “trapped” scores of new candidate substrates of the protease ClpXP to reveal how protein degradation is critical to cell cycle progression and bacterial development. The new understanding could lead to identifying new antibiotic targets.
Researchers led by M. Mahmood Hussain, PhD, found that a regulatory RNA molecule interferes with the production of lipoproteins and, in a mouse model, reduces hyperlipidemia and atherosclerosis.
A major study from researchers at the La Jolla Institute for Allergy and Immunology provides new revelations about the intricate pathways involved in turning on T cells, the body’s most important disease-fighting cells, and was published today in the prestigious scientific journal Nature. The La Jolla Institute team is the first to prove that a certain type of protein, called septins, play an essential role in T cell activation.
Development of skin cancer may require changes in the genes that control cell shape, report a team of scientists from three institutions in an upcoming issue of Nature Cell Biology. The work could lead to a better understanding of how the cells become metastatic.
Scientists have discovered the survival secret to a genetic mutation that stokes leukemia cells, solving an evolutionary riddle and paving the way to a highly targeted therapy for leukemia. In a paper published today in Cell, researchers at NYU Langone Medical Center describe how a mutated protein, called Fbxw7, behaves differently when expressed in cancer cells versus healthy cells.
Better treatments for people suffering from compromised intestinal immunity may emerge from a small-animal model of human intestinal immune development.
In this week’s issue of Nature, scientists at The Scripps Research Institute report their discovery of an important trick that a well-known intrinsically disordered protein uses to expand and control its functionality.
A team from the New York Stem Cell Foundation (NYSCF) Research Institute and the Naomi Berrie Diabetes Center of Columbia University has generated patient-specific beta cells, or insulin-producing cells, that accurately reflect the features of maturity-onset diabetes of the young (MODY).
Memory improved in mice injected with a small, drug-like molecule discovered by UCSF San Francisco researchers studying how cells respond to biological stress.
In an article published in the Proceedings of the National Academy of Sciences (PNAS) a research team from University of North Carolina at Charlotte announced that they had uncovered a previously unknown surveillance mechanism, known as a DNA damage checkpoint, used by cells to monitor oxidatively damaged DNA. The finding, first-authored by UNC Charlotte biology graduate student Jeremy Willis and undergraduate honors student Yogin Patel, was also co-authored by undergraduate honors student Barry L. Lentz and assistant professor of biology Shan Yan.
Scientists at The Scripps Research Institute have identified key triggers of an important cancer-blocking mechanism in cells. Termed “oncogene-induced senescence,” this mechanism can block most cancer types and is commonly experienced when incipient skin cancers turn instead into slow-growing moles.
Scientists at North Carolina State University have found the first example of how micro-RNA regulates wood formation inside plant cells and mapped out key relationships that control the process.
Biologists from Indiana University and Montana State University have discovered a striking connection between viruses such as HIV and Ebola and viruses that infect organisms called archaea that grow in volcanic hot springs. Despite the huge difference in environments and a 2 billion year evolutionary time span between archaea and humans, the viruses hijack the same set of proteins to break out of infected cells.
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