Researchers have identified a new function for APJ protein in sensing mechanical changes that can lead to heart failure. Without this protein, the heart is less likely to sense danger and undergo hypertrophic pathways leading to heart failure.
Researchers develop miR-TRAP, a new method to directly identify microRNA targets in cells. This technique allows scientists to understand the roles microRNAs play in human development and disease, bridging a gap in the RNA field.
Researchers at Sanford-Burnham Medical Research Institute found that MLN4924-resistant cancer cells escape death due to a simple mutation in the NEDD8-activating enzyme. The team developed a method to predict how cancer patients will respond to this drug, providing a new path toward personalized medicine.
Researchers at Sanford-Burnham discovered a chemical compound that inhibits the mutant form of LYP, a protein implicated in multiple autoimmune diseases. The findings suggest a new potential therapy for autoimmune diseases, including Type I diabetes and rheumatoid arthritis.
A genome-wide study identified 190 genes critical for the function of TLR7 and TLR9, cellular sensors that recognize pathogens and trigger immune responses. The findings provide insights into the complex network regulating immune responses to microbial infections.
Research on multiple hereditary exostoses (MHE), a rare genetic disease, reveals the molecular basis of autistic symptoms in children with MHE. The study identifies the amygdala as the brain region responsible for autistic symptoms, shedding light on potential underlying causes and future treatments.
Sanford-Burnham researchers discovered the first 3D structure of the botulinum neurotoxin and its protein bodyguard. This reveals a weak spot that can be targeted to develop new therapeutics, including potential treatments for botulism and bioterrorism agents.
Researchers at Scripps Research and Sanford-Burnham Medical Research Institute have determined the 3D structure of the interaction between an immune molecule called TLR5 and a protein that helps bacteria move. This breakthrough provides significant insights into the molecular mechanism underlying TLR5 recognition and function.
Researchers developed a new mouse model to study medulloblastoma, a devastating childhood brain cancer. The model suggests a potential strategy to inhibit tumor growth using PI3-kinase inhibitors, which have shown significant increases in mouse survival.
Researchers at Sanford-Burnham Medical Research Institute discovered that beta cells in the pancreas use taste receptors to sense fructose, a type of sugar. This finding suggests that fructose plays a role in insulin release, amplifying the effect of glucose and potentially impacting metabolic diseases like obesity and diabetes.
A new study at Sanford-Burnham Medical Research Institute suggests that the heart hormone natriuretic peptides play a role in breaking down fat. The peptides turn on a molecular mechanism similar to what's activated when the body is exposed to cold and burns fat to generate heat.
Researchers at Sanford-Burnham identified a molecular switch, controlled by protein kinase C-epsilon, that enables melanoma cells to resist chemotherapy. High levels of PKC-epsilon in melanoma are associated with poor prognosis and increased tumor-promoting activity.
Researchers found that antipsychotics activate the TGFbeta pathway, leading to metabolic side effects, while drugs without these effects do not. The study suggests a new approach to developing safer therapeutics for bipolar disorder and schizophrenia patients.
Researchers at Sanford-Burnham Medical Research Institute discovered a way to reprogram muscle cells to burn sugar more efficiently, resulting in increased athletic ability and reduced lactic acid production. This novel mechanism could lead to new prevention or treatment methods for obesity, metabolic syndrome, and diabetes.
A team of scientists at Sanford-Burnham Medical Research Institute has developed a new method for delivering cancer drugs directly to tumors, reducing side effects and increasing effectiveness. The technique uses a tumor-homing peptide that targets blood vessels feeding tumors, allowing the drug to be administered with minimal impact o...
Scientists at Sanford-Burnham Medical Research Institute discovered a protein called Siah2 that regulates mitochondrial fragmentation under low oxygen conditions. Inhibiting Siah2 prevents heart cell death and reduces tissue damage in mice, suggesting a new therapeutic target for heart disease treatment.
Researchers at Sanford-Burnham Medical Research Institute have identified a new component of the cellular machinery that senses dietary amino acids, which is essential for mTORC1 activation. This finding provides new information about mTORC1 and its role in cellular metabolism in both normal cells and cancer cells.
Scientists at Sanford-Burnham discovered that orexin activates calorie-burning brown fat in mice, suggesting potential for new obesity treatments. The hormone is associated with increased energy expenditure and weight loss.
Scientists at Sanford-Burnham and Salk Institute developed a method to combine peptides and nanoparticles to eliminate glioblastoma in previously untreatable mouse models. The nanosystem proved effective in treating two different mouse models, curing most tumors and significantly delaying tumor development.
Researchers found that increased autophagy in germline-less worms led to higher activity of a fat-digesting enzyme, extending their lifespan. The study suggests that recycling fat is beneficial for worms, and may have implications for human diseases such as cancer and Alzheimer's.
A study by Sanford Burnham Prebys reveals that CDP138 is a crucial protein for insulin-stimulated glucose uptake in muscle and fat cells. The researchers found that optimal insulin response requires the correct insertion of GLUT4 into the cellular membrane, with CDP138 playing a key role.
A modified form of the enzyme Cdk5 is elevated in Alzheimer's disease patients, triggering damage to nerve cell connections. This discovery suggests that SNO-Cdk5 could be targeted for the development of new Alzheimer's disease therapies.
A new study found that high levels of fat interfere with key transcription factors, leading to diminished glucose sensing in pancreatic beta cells. This pathway is activated in type 2 diabetes and contributes to metabolic defects, including insulin resistance.
A high-throughput screen identified several compounds that inhibit invadopodia formation, a key step in cancer cell invasion. In contrast, another compound, paclitaxel, was found to promote invadopodia formation and cancer cell invasion.
Research reveals that long non-coding RNA SPRY4-IT1 promotes cellular survival and invasion in melanoma cells, suggesting its potential as an early biomarker. The study also found reduced levels of another non-coding RNA, miR-211, in melanoma cells.
A study by Dr. Alexey Terskikh and colleagues found that the SOX2 gene maintains the potential for neural crest stem cells to become neurons in the peripheral nervous system. This discovery could help inform therapies for neurocristopathies, diseases caused by defects in the neural crest or neurons.
A study published in Cell Metabolism identifies a previously underappreciated cellular fat storage depot controlled by sterol regulatory element-binding protein 2 (SREBP-2), which plays a crucial role in balancing cellular cholesterol levels and regulating autophagy.
Researchers developed induced conditional self-renewing progenitor cells, which can differentiate into active neurons and other brain cell types. The new stem cell approach shows promising results in an adult rat model of intracerebral hemorrhagic stroke, with no adverse effects observed over five months.
Researchers created a computer program that predicts the lifespan of hematopoietic stem cells, finding that each cell has a set amount of time for self-renewal. This understanding can improve the safety and efficacy of bone marrow transplants and potentially lead to breakthroughs in regenerative medicine.
A team at Sanford-Burnham identified specific microRNAs that enhance the reprogramming process from skin cells to induced pluripotent stem (iPS) cells. Adding these miRNAs increases cell survival and improves iPS cell generation.
Researchers at Sanford-Burnham Medical Research Institute have discovered a genetic mechanism that causes lipotoxic cardiomyopathy independently of a diet high in fat. The study found that an imbalance in cellular fats can lead to heart problems, and targeting the SREBP protein may help prevent these issues.
Researchers at Sanford-Burnham Medical Research Institute have unraveled the relationship between MITF and ATF2, a transcription factor involved in melanoma development. The study reveals that the ratio of ATF2 to MITF in melanoma cells can predict survival in melanoma patients.
A new study reveals that a key muscle protein is necessary for exercise but not normal muscle development. PGC-1-deficient mice exhibit mitochondrial problems but remain insulin-sensitive and do not develop diabetes.
A recent study in fruit flies discovered a molecular connection between obesity and heart disease, with the protein TOR playing a key role. Researchers found that manipulating TOR protected the hearts of obese flies from damage caused by high-fat diets.
A new study reveals that the protein T-cadherin is necessary for adiponectin's cardioprotective functions. Adiponectin activates AMPK, which regulates energy usage in the cell. The absence of T-cadherin leads to impaired AMPK activity and increased cardiac damage.
A new study finds that SHIP and PTEN proteins act cooperatively to suppress B cell lymphoma. The research could lead to the development of new anti-lymphoma drugs targeting PI3K signaling.
A recent study published in The Journal of Neuroscience explains the unique molecular action of memantine, a FDA-approved drug for Alzheimer's disease, that underlies its rare side effects. Memantine improves symptoms by blocking abnormal glutamate activity, sparing synaptic receptors and minimizing harm.
Researchers found that a gaseous molecule called nitric oxide can trigger brain cell death in neurodegenerative diseases. The study discovered a new molecular pathway that leads to cellular suicide, offering new potential for diagnosis and treatment.
A recent study reveals that the JNK protein controls the cell cycle by regulating key drivers of cell growth. The findings suggest that hyperactive JNK activity may contribute to genomic instability and promote tumor growth.
A team of investigators has identified a series of proteins that may make it easier to diagnose the more metastatic forms of prostate cancer. The study uncovers a protein named Siah2, which initiates a cascade of molecular events that turns a non-malignant tumor into a metastatic neuroendocrine tumor.
Researchers at Sanford-Burnham Medical Research Institute have discovered a new application for the painkiller Sulindac as a potential anti-cancer treatment. By binding to the truncated form of nuclear receptor RXRα, Sulindac shuts down cancer cell growth and initiates cell death.
Researchers at Sanford-Burnham Medical Research Institute created a new mouse model of multiple hereditary exostoses, a rare childhood disease characterized by abnormal bone growths. The study reveals the molecular basis of the disease and provides a tool to screen new treatments.
Recent discoveries may help curb anti-apoptotic proteins that tumors express to resist treatment. Researchers outline how six anti-apoptotic proteins in the Bcl-2 family are expressed differently in different cancers.
Researchers discovered a peptide called iRGD that co-administers drugs to tumors, increasing treatment efficacy and reducing side effects. The peptide has been shown to enhance the therapeutic effect of anti-cancer drugs without creating new chemical entities.
A study has identified genes that contribute to heart function and disease, shedding light on the genetic underpinnings of heart disease. The researchers found nearly 500 genes associated with heart problems in flies, including a protein complex called CCR4-Not.
Researchers discovered that sceptrin reduces cancer cell motility and limits cell contractility, a critical function for cell movement. The naturally-derived compound and its synthetic version showed effectiveness in combating metastasis in various cancer types.
A team of researchers has discovered the mechanism behind Frank-Ter Haar syndrome, a rare fatal disorder that affects children's skeletal, cardiovascular, and eye health. The study identified TKS4 as a critical protein involved in the condition.
Researchers demonstrate that transplanted stem cells can rescue diseased neurons from death by sending signals through gap junctions, a newly recognized way of cell communication. This mechanism may play a role in both normal development and many diseases, including Huntington's disease and spinal cord injuries.
Researchers at Sanford-Burnham Medical Research Institute have identified a new function of the CD44 receptor, which helps specific T helper cells develop immunologic memory. This discovery could lead to the development of therapies to control disease pathology in various infections and autoimmune conditions.
Investigators at Burnham Institute for Medical Research identified 295 human cell factors that influenza A strains must harness to infect a cell. The team also found small molecule compounds that act on several of these factors and inhibit viral replication, pointing to new ways to treat flu.