Articles tagged with Cell Death
Scientists at WashU Medicine identified three unexpected players, small RNA molecules, that help a cell initiated its own demise when overloaded with fat. The research links these molecules to the cellular damage characteristic of common metabolic diseases like diabetes.
Researchers at Rutgers University have identified P75 as a likely culprit in post-seizure brain cell death, which can benefit people with epilepsy and those suffering from traumatic brain injuries and strokes. The study aims to prevent cell death by testing molecules that block the P75 receptor.
Researchers have uncovered how yeast cells recognize and assemble cargo mRNA for transport, a process critical for cell function. The discovery sheds new light on the mechanisms underlying molecular transport in both simple and complex organisms.
Researchers found that the process of repairing damaged DNA repeats can lead to cell death in yeast, providing insight into neurodegenerative diseases. The study suggests that expanded DNA repeats can be toxic to cells, contributing to disease progression.
Researchers at UC Riverside have identified a chemical compound, blebbistatin, that inhibits the molecular motor NMII and prevents cell death in human pluripotent stem cells. This breakthrough discovery brings stem cell research closer to finding therapies for various diseases.
Scientists at the Brain Research Centre have discovered a new mechanism for brain cell death after a stroke, involving the over-activation of NMDA receptors and a protein called SREBP-1. A potential therapy has been found, using a drug that stabilizes Insig-1 to inhibit SREBP-1 activity.
A Purdue University researcher has discovered that increasing protein phosphatase 5 (PP5) in neurons reduces reactive oxygen species-induced cell death, a mechanism linked to Alzheimer's disease. PP5 overexpression also prevents amyloid beta-mediated stress pathways.
University of Cincinnati researchers have identified a specific step in the biological chain of events leading to Diamond Blackfan anemia. They discovered that a ribosomal protein defect leads to abnormal activation of p53, causing premature death of red blood cells.
Researchers found that blocking Cyclophilin D and developing surrounding mitochondrial targets may be viable strategies for preventing and treating Alzheimer's disease. The study provides new insights into the mechanism underlying amyloid beta-mediated mitochondrial stress, which links to synaptic plasticity and learning/memory.
Researchers at the University of Montreal have discovered a potential new treatment for cardiac complications in Duchenne muscular dystrophy patients. The study, published in the Proceedings of the National Academy of Sciences, shows that administering sildenafil protects the heart in mice with the disease.
A study by University of Iowa researchers reveals a new dimension for a key heart enzyme and sheds light on an important biological pathway involved in cell death in heart disease. The team found that oxidation can sustain the enzyme's activity, which is implicated in arrhythmias, hypertrophy, and heart cell death.
Researchers at Ohio State University Medical Center found that the mitochondria send a death signal to cardiac cells when blood flow is restored, leading to cell damage and weakening heart function. The study identifies a specific enzyme, mitochondrial nitric oxide synthase, as a potential therapeutic target to stop this process.
Researchers found that inactivating TNFa significantly reduced blood vessel impairment and cell death in aged vessels, suggesting a link between increased TNFa levels and cardiovascular disease. The study's findings could lead to the development of new treatments for age-related vascular diseases.
Researchers found transcription factor Elk-1 localized in dendrites of neurons, affecting cell viability. Overexpressing Elk-1 decreased cell viability, while knocking down expression increased neuron survival.
Researchers found that cytotoxic T lymphocytes (CTLs) kill only a fraction of infected cells, with most deaths attributed to other factors. The study suggests that CTL-based vaccines may not prevent or clear HIV infection and could control the number of infected cells instead.
Researchers at Washington University School of Medicine in St. Louis have identified EF1A-1 as a critical step in the pathway leading to high cellular fat and cell death. The protein plays a role in protein synthesis and cytoskeleton maintenance, and its presence dictates sensitivity to palmitate-induced cell death.
Researchers found that over half of the 46 known microRNAs are essential for development, affecting it in specific ways. MicroRNAs regulate fundamental processes such as body patterning, morphogenesis, and nervous system development.
Researchers have made significant breakthroughs in understanding a natural mechanism cells use to protect themselves from stress, with potential applications for preventing motor nerve cell death. Up to 50% of nerve cell death could be prevented in mice with sciatic nerve injury using this approach.
A recent study published in Molecular Psychiatry reveals that cell death promotes learning and growth in the brain. The research found that rats with lower levels of cell death performed better in spatial learning tasks, suggesting a positive correlation between cell death and cognitive function.
Researchers found that cardiac MRI technology can detect small areas of heart muscle death that are missed by traditional nuclear imaging techniques like SPECT. This is important because these microinfarcts can be early indicators of future severe heart problems.
Researchers have discovered a new way to prevent cell death in the brain, which could lead to treatments for stroke, schizophrenia, and other neurological disorders. By enhancing the interaction between two proteins, they may be able to design medications that target specific brain functions.
Researchers discovered how E. coli O157:H7 causes massive cell death in humans, leading to organ failure and death. The bacteria's verotoxins trigger programmed cell death through a Bcl-2 protein sequence, offering potential new treatments for food poisoning.
Researchers at University of Toronto have identified a common principle underlying brain cell death in neurodegenerative disorders. They propose a 'one-hit' model, where cells die after a single catastrophic event, rather than gradual damage over time.