Researchers found that reduced levels of SNX27 protein lead to increased beta-amyloid production and brain plaques, a hallmark of Alzheimer's disease. Adding new copies of the SNX27 gene can repair memory deficits in Down syndrome mice.
Researchers at Sanford-Burnham Medical Research Institute have developed a novel technique to promote tissue repair in damaged muscles. Cyclic bursts of a STAT3 inhibitor can replenish muscle stem cells, leading to their differentiation into muscle fibers, which could provide a new therapeutic approach to treating muscle diseases.
Researchers at Sanford Burnham Prebys Institute have discovered a promising technique to restore insulin production in people with Type 1 diabetes. A peptide called caerulein was found to convert existing alpha cells into insulin-producing beta cells, potentially freeing patients from daily insulin doses.
A new study by Sanford-Burnham researchers identifies the NBR1 protein as a critical regulator of obesity-induced inflammation, which leads to metabolic disease. The study suggests that blocking this signal may protect against the development of metabolic disease and type 2 diabetes.
Researchers at Sanford-Burnham Medical Research Institute have identified a chemical switch controlling neuron generation and survival in the brains of Alzheimer's patients and stroke victims. This switch, MEF2, may be a potential therapeutic target to protect against neuronal loss in various neurodegenerative diseases.
A team of scientists found that losing p62 in surrounding cells enhances tumor growth and progression. The study suggests therapies targeting the tumor microenvironment may be as important as targeting the tumor itself.
A collaborative study has identified two oncogenes, GFI1 and GFI1B, that drive the development of medulloblastoma, the most common malignant brain tumor in children. The findings suggest these genes are worthy candidates for molecular-targeted therapy.
Researchers have discovered a synthetic molecule that inhibits T-cell signaling in the lungs, preventing asthma symptoms such as inflammation and airway constriction. The molecule shows promise for treating asthma, a chronic disease affecting over 25 million Americans.
A team of scientists has published a study revealing novel cellular and molecular elements of muscle repair. Researchers found that HDACis drugs create an environment conducive for FAPs to direct muscle regeneration in early stages of Duchenne muscular dystrophy, but fail to work later.
Sanford-Burnham will present various cancer research findings at the AACR annual meeting, including novel methods of drug delivery and novel targets for breast, melanoma, and prostate cancers. Researchers will also discuss epigenetic mechanisms and cancer metastasis.
A team of scientists has identified a key factor that contributes to neurodegeneration in ataxia-telangiectasia, a rare genetic disorder. The study found that DNA damage repair systems are essential for cellular integrity and stability, and that defects in these systems can lead to conditions like A-T.
Researchers have successfully implanted encapsulated human embryonic stem cell-derived pancreatic cells under the skin of animal models with diabetes, producing sufficient insulin to maintain glucose levels. The study suggests that these cells may be a promising treatment option for insulin-dependent diabetes.
Researchers at Sanford-Burnham and Icahn School of Medicine at Mount Sinai have discovered a key cellular process leading to heart failure, which can be halted with a therapeutic approach. Blocking the effects of miR-25 has improved cardiac function and survival in mice.
Sanford-Burnham researchers identify THRIL molecule that regulates immune response and associates with Kawasaki disease severity. THRIL may also contribute to other inflammatory diseases like rheumatoid arthritis and inflammatory bowel disease.
Scientists at Sanford-Burnham have identified the B and T Lymphocyte Attenuator (BTLA) inhibitory receptor as a key factor in limiting inflammatory responses, particularly in the skin. The study provides clarity on how T cells get fired up to protect against pathogens, and then cool down to restore immune homeostasis.
Researchers used patient-derived stem cells to show that a genetic mutation in the alpha-synuclein gene increases vulnerability to pesticides, leading to Parkinson's disease. The study identified a molecule that protects neurons from pesticide damage and may have potential clinical implications for treating the disease.
The institute will utilize its high-throughput, human cell-based assays and induced pluripotent stem cells to analyze thousands of potential toxins. This collaboration aims to provide an early and relevant assessment of potential toxicities in a rapid and cost-effective manner.
Researchers developed a new method to treat medulloblastoma by disrupting cancer stem cells, halting their ability to proliferate. The approach shows promise in preventing tumor progression and overcoming resistance to therapy, offering hope for patients with this highly malignant cancer.
Researchers identify phosphoinositide-dependent kinase-1 (PDK1) as a critical regulator in melanoma development and metastasis. Inhibiting the PDK1 enzyme delays tumor growth and almost completely abolishes metastasis, offering new therapeutic opportunities for this life-threatening disease.
Researchers at Sanford-Burnham Medical Research Institute have identified a critical transcription factor that regulates autophagy, a cleansing mechanism for cells. The discovery could lead to new therapies for age-related disorders by inducing autophagy in animal models and dietary-restricted mice.
Researchers at Sanford-Burnham Medical Research Institute have uncovered a new metabolic pathway that regulates cell growth and responds to nutrients such as amino acids and glucose. The pathway involves the protein p62 and its interaction with TRAF6, which activates mTORC1 in response to nutrient signals.
Researchers at Sanford-Burnham Medical Research Institute have identified a novel mechanism of action for SMIP004, which specifically kills prostate cancer cells by interfering with mitochondrial function. The compound's effects were found to be particularly promising for treating castration-resistant prostate cancer.
Researchers at Sanford-Burnham Medical Research Institute have developed nanoparticles that can deliver small interfering RNA molecules to specific cells, effectively silencing malfunctioning genes. The approach points toward new ways to treat diseases such as cancer and heart disease by using RNA interference.
Researchers at Sanford-Burnham Medical Research Institute developed a new drug, NitroMemantine, that boosts brain synapses lost in Alzheimer's disease. The drug restores synaptic connections between nerve cells, offering new hope for early and late-stage Alzheimer's patients.
A study found that rod-shaped nanoparticles adhere effectively to endothelial cells, enhancing drug delivery. Researchers believe this technology holds promise for novel targeted therapies with fewer side effects.
Researchers have identified Dkk1 as a key player in the development of atherosclerosis, a condition that causes arteries to become stiff and narrow, leading to impaired blood flow. Targeting Dkk1 signaling may help limit arteriosclerotic disease, according to a new study.
Researchers at Sanford-Burnham Medical Research Institute discovered that three children with Congenital Disorders of Glycosylation had mutation-only in some cell types, raising questions about inheritance and genomic sequencing. The study highlights the importance of using multiple diagnostic tests to accurately diagnose rare diseases.
A study published in The Journal of Clinical Investigation found that microRNAs play a crucial role in determining muscle fitness by regulating the switch between slow- and fast-twitch muscle fibers. The researchers identified specific microRNAs that are elevated in active people, suggesting a potential new target for interventions to ...
Researchers at Sanford-Burnham discovered an imbalance between neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. In mouse models and human studies, reversing this imbalance protected against weight gain, metabolic problems, and inflammation.
Researchers at Sanford-Burnham Medical Research Institute discovered that the enzyme PKCζ acts as a tumor suppressor in both mice and humans, controlling cell growth and metastasis. Restoring PKCζ levels may provide a novel therapeutic target for treating prostate cancer.
Researchers found that the extra chromosome 21 leads to reduced SNX27 protein levels, disrupting brain function. Restoring SNX27 in Down syndrome mice improves cognitive function and behavior.
A study by Sanford-Burnham researchers found that Siah2 keeps androgen receptors constantly active in prostate cancer cells, enabling them to survive treatment. Inhibiting Siah2 may provide a new method for re-sensitizing castration-resistant prostate tumors to hormone therapy.
Researchers at Sanford-Burnham Medical Research Institute have determined the complete three-dimensional structure of HNF-4alpha protein, a key player in rare diabetes. The study reveals new pockets that could be targeted with therapeutic drugs to alleviate MODY1 symptoms.
Researchers discovered nitric oxide inhibits ERK1/2 signaling pathway, shutting down brain's ability to self-repair after stroke. The study found that excessive nitric oxide production contributes to the severity of stroke and other neurological disorders.
Researchers at Sanford-Burnham Medical Research Institute discovered that tumors lacking the protein PKCζ can survive on alternative nutrients. The study suggests glucose depletion therapies may work against these tumors as long as they produce PKCζ, which is responsible for tumor metabolism.
Scientists develop the first maturation-based disease model for arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) using patient skin cells. The model mimics adult-onset disease by inducing adult-like metabolism, revealing metabolic malfunction and abnormal protein activation as key drivers of the disease.
Researchers used fruit flies to model diet-induced type 2 diabetes, revealing a specific biochemical system linked to the condition. Blocking this pathway prevents some of the disease's negative effects on the heart, providing new avenues for therapy.
Researchers discover that belly and thigh fat differ significantly in gene expression, with unique homeobox genes influencing fat cell behavior. This finding may lead to targeted treatments for obesity, shifting focus from belly fat to hip and thigh fat.
Sanford-Burnham researchers discover that protein p62 plays a crucial role in balancing metabolism in fat tissue. When p62 is missing, the body's metabolic balance shifts towards 'bad' white fat and away from 'good' brown fat. This finding indicates that p62 could be an attractive target for new therapies aimed at curbing obesity.
In a groundbreaking study, researchers found that transplanted neural stem cells slow ALS disease onset and progression by producing protective molecules and reducing inflammation. The treatment improves motor function and prolongs survival in ALS mice, offering new hope for treating this devastating disease.
Sanford-Burnham researchers found that two microRNA families, let-7 and miR-18, regulate germ layer formation by dampening the TGFβ signaling pathway. This discovery provides a paradigm for whole-genome screening and its use in identifying molecular signals controlling complex biological processes.
Scientists at Sanford-Burnham Medical Research Institute have discovered that carnosic acid, a component of rosemary, promotes eye health and protects retinas from degeneration. The findings suggest a possible new approach for treating age-related macular degeneration.
Researchers at Sanford-Burnham Medical Research Institute have successfully transplanted human stem cell-derived neurons into a rodent hippocampus, stimulating existing neurons to fire high-frequency oscillations. This breakthrough may lead to the restoration of brain activity and motor function in patients with neurodegenerative condi...
Sanford-Burnham researchers found that different brain tumor cell types respond to distinct treatments due to varying growth factor regulation. This discovery offers potential for more effective and less harmful treatments tailored to individual tumors.
Researchers at Sanford-Burnham Medical Research Institute have developed a new method to generate induced pluripotent stem cells (iPSCs) by adding kinase inhibitors, which significantly increase cellular reprogramming efficiency. This breakthrough has the potential to accelerate disease research and drug development.
Duc Dong, Ph.D., receives NIH New Innovator Award to explore genetic reprogramming as a means to grow replacement organs. The technology aims to induce new tissue development in zebrafish, allowing for rapid screening of genes and chemicals important for efficient genetic reprogramming.
Huei-Sheng Vincent Chen, PhD, receives $1.58 million CIRM Basic Biology IV award to develop personalized models of inherited heart conditions using stem cells derived from patients' own skin cells. The goal is to develop new therapies for these diseases and better understand their causes.
Researchers at Sanford-Burnham Medical Research Institute discovered that BACE1 disrupts cellular processes required for PKA function, leading to impaired learning and memory. This finding suggests that targeting BACE1 expression in the brain could be a potential therapy for Alzheimer's disease and age-related memory loss.
Scientists at Sanford-Burnham Medical Research Institute found a molecule that promotes tumor vessel maturation, which could improve the effectiveness of anti-cancer therapies. By boosting R-Ras activity, researchers aim to normalize blood vessel structure and function in tumors, enabling better drug delivery.
Researchers at Sanford-Burnham Medical Research Institute have discovered a molecule that converts stem cells into heart cells, potentially replacing diseased or damaged tissue in heart disease patients. The molecule, ITD-1, blocks TGFϐ signaling, allowing stem cells to differentiate into cardiomyocytes.