Articles tagged with Redox Signaling
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Reactive oxygen species (ROS) homeostasis is essential for cellular survival and physiological functions. The review discusses its biological significance, potential clinical applications, and regulatory mechanisms underlying ROS homeostasis. Dysregulation of ROS homeostasis is a common pathogenic mechanism driving disease development.
A study has discovered a connection between ferroptosis, a type of iron-dependent cell death, and inflammatory bowel disease. Lipid ROS activate ferroptosis, which drives cell death in the colon lining, and inhibiting this process may lead to new treatment options for IBD.
A new nanomedicine, ZnDHT NM, selectively targets cancer stem-like cells (CSCs) and tumor cells, promoting CSC differentiation while inhibiting EMT. This approach also leads to the release of toxic compounds in tumor cells, inducing apoptosis/ferroptosis pathways.
Overexpressing hepatic SLC7A11 leads to glutamate and serine deficiency, promoting MASLD progression through ferroptosis. Serine supplementation rescues the disease phenotype.
Scientists have developed genetically encoded biosensors to measure the ratio of NADPH to NADP⁺ in real-time, revealing new insights into cellular detoxification and protective function.
A novel 'reporter' molecule has been developed to detect ER-related problems during protein synthesis, offering simplicity and robustness against environmental fluctuations. The tool uses a firefly luciferase-based system to identify defects in protein translocation and disulfide bond formation.
Researchers at the University of São Paulo have discovered a way to detect peroxymonocarbonate, a potent oxidant derived from CO2, in human cells. The novel method uses fluorescent molecular probes and has implications for understanding the impact of high CO2 levels on human health.
Researchers found that Angelica gigas extract improves vascular function in high-fat diet rats, reversing endothelial dysfunction and increasing NO bioavailability. The extract regulates IRE1α sulfonation and RIDD signaling, promoting NO production via the SIRT1-eNOS axis.
Researchers at the University of Illinois have developed a copolymer system that can control solvation and bind different ions through an electrochemical process. The study presents a new pathway for electrochemically controlling ion selectivity, offering a precise platform for removing ions from water.
Research suggests visfatin stimulates membrane raft clustering, leading to NLRP3 inflammasome activation and podocyte injury. The study highlights the role of membrane raft redox signaling in visfatin-induced inflammation and kidney damage.
A recent study found that transient inflammatory pain causes persistent mitochondrial and metabolic disturbances in sensory neurons, leading to failure in pain resolution. Targeting the cellular redox balance prevents and treats chronic inflammatory pain in rodents.
X- and y-type thioredoxins play a crucial role in maintaining the redox balance of photosynthesis during fluctuating light conditions. The study found that these proteins facilitate electron transport through the electron transport chain, preventing photoinhibition and promoting plant growth.
Bacteria can regulate nitrogen fixation through a protein called NifL, which changes shape in response to oxygen and energy levels. This discovery could lead to new ways to engineer bacteria and biofertilizers, improving crop yields in poor soils.
Researchers discovered 'oxygen hole' formation in LiNiO2 cathodes accelerates degradation and release of oxygen. Computational studies revealed nickel charge remains stable while oxygen undergoes changes during charging.
Researchers at Buck Institute for Research on Aging developed a bioavailable compound that selectively inhibits free radical production in mitochondria, preventing and treating metabolic syndrome in mice. The compound, S1QEL1.719, decreases fat accumulation, improves glucose tolerance, and normalizes fasting insulin levels.
A study by Juntendo University researchers reveals that p62 bodies control redox-independent NRF2 activation through phosphorylation of ULK1, enabling the antioxidative stress response. The finding provides new insights into the role of phase separation in stress responses and its physiological significance.
A team of researchers used synchrotron XRD to investigate the topochemical solid-gas reduction mechanisms in a layered perovskite. The study found that surface treatment can manipulate reaction processes, and the technique can identify rate-determining steps for optimizing material design.
Researchers found 560 proteins were differentially expressed, with 32 significantly altered, in reductive stress hearts. The proteome signature revealed oxidative stress-related pathways and mitochondrial dysfunction.
Leukemia cells exploit metabolic pathways to evade programmed cell death, but researchers identified a weak spot in acute lymphoblastic leukemia that can be targeted with experimental drugs. Inhibiting glutathione metabolism induces ferroptosis, leading to the death of malignant lymphocytes.
Researchers found that suppressing an enzyme called MSRA, which fixes oxidative damage to proteins, sparks the metastatic spread of pancreatic cancer cells. The discovery suggests that similar switches may exist in other cancers and lays the groundwork for redox-based targeted therapies.
The 24th International Conference on Oxidative Stress Reduction, Redox Homeostasis & Antioxidants, shed light on the latest redox field innovations and the future of redox medicine. Keynote speaker Prof. Helmut Sies discussed stringently selective modulation of enzymatic oxidant sources and sinks in redox nanomedicine.
Academic researchers will present newest discoveries on redox in aging, immunity, ocular disorders, and fertility. The conference highlights the mechanisms of redox control like Nrf2 signaling pathway.
A study suggests that the powerhouse-pruning protein Drp1 plays a crucial role in generating energy for new blood vessel growth, particularly under low oxygen conditions. When oxygen levels are low, Drp1 gets modified to produce reactive oxygen species (ROS), which enables glycolysis and subsequent cell signaling.
A team of scientists has observed direct atomic evidence of the anionic redox mechanism in lithium-rich cathodes, which could lead to breakthroughs in battery technology. The discovery provides conclusive evidence for this mechanism, nearly doubling the energy storage capacity compared to conventional cathodes.
Researchers have developed a nondestructive way to measure drug treatment responses in lab-grown cancer samples using redox imaging. The technique allows for sensitive information about drug responsiveness and can identify organoid subpopulations with distinct responses.
Researchers have found that reductive stress promotes protein aggregation and impaired neurogenesis in neuroblastoma cells. This suggests a new role for reductive stress in the onset and progression of neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's.
Researchers create tiny communication networks that allow electronics to eavesdrop on cells and alter their behavior. These systems could enable applications such as wearable devices for bacterial infections and capsules for tracking blood sugar levels.
Researchers at UMD are using CRISPR technology to create microelectronic devices that can electronically turn genes on and off. This technique has the potential to bridge the gap between biology and electronics, enabling new wearable and smart devices.
Researchers at UC Davis have identified novel inhibitors that can disrupt redox signaling to prevent haustorium initiation in parasitic plants. This breakthrough could lead to new control methods against economically damaging agricultural pests.
Moffitt researchers identified three subtypes of squamous cell lung cancer (SCC) with distinct genetic, chromosomal, and protein alterations. The inflamed subtype is characterized by immune cell infiltration and higher PD-1 levels, while the redox subtype has altered oxidation-reduction signaling pathways. These subtypes did not correl...
A recent study published in Science Signaling reveals that the ATM protein plays a dual role in sensing cellular threats and repairing damage. It forms dimers when exposed to ROS, triggering an increase in cellular antioxidant capacity through the pentose phosphate pathway.
Researchers have discovered a new mechanism by which mitochondria regulate protein synthesis in response to oxidative stress. Using quantitative mass spectrometry and biochemical methods, the team identified redox-active thiols that can slow down cellular protein synthesis machinery when reactive oxygen species are present.
A study published in Cell Chemical Biology discovered a novel chemical procedure called T-REX that can selectively target cancer cells with specific mutations, leading to more favorable treatment outcomes. The researchers found that certain enzymes' redox-specific processes could be harnessed for targeted drug design.
A new regulatory mechanism has been identified that allows animals to increase reductive power in response to high sugar intake. This mechanism involves protein kinase SIK3 and glucose metabolism enzyme G6PD, providing protection against oxidative stress and allowing for conversion of excess sugar into fat.
Researchers at Joslin Diabetes Center found that the protein IRE-1 can react to ROS molecules, triggering an antioxidant response that increases cell resistance to stress. This discovery highlights the need to consider ROS molecules as links in cell pathways, not just as damaging agents.
Copper influx is crucial for brain cell development, allowing for the rapid transport of copper to activate enzymes and facilitate signaling between neurons. This study reveals how cells adjust copper allocation from energy production to enzyme activation as they mature.
A new compound developed at the University of Toronto Scarborough can monitor protein kinase activity without using radioactive isotopes. This innovation has potential to improve cancer treatment by providing a safer and more accurate method for assessing drug effectiveness.
Researchers developed a new optical microscopy technique to analyze the redox state of mitochondria in living tissue. The study revealed that severance of an axon results in a wave of oxidation of the mitochondria, which begins at the site of damage and is propagated along the fiber.
Research team discovers changes in glutathione redox potentials between cytosol and mitochondria, indicating different redox requirements for each compartment. Inhibition of GSH synthesis leads to increased mitochondrial oxidation in response to GSH depletion.
Researchers have charted a significant signaling network in Synechococcus, a fast-growing microbe that can produce biofuels. The findings reveal redox reactions that allow the organism to adapt to changing environments and provide insights into its ability to create biofuels.
Researchers discovered that tumor suppressor genes TSC and PTEN regulate stem cell-like blood precursor cells in fruit flies. The TOR pathway uses these genes to gauge nutrition levels and stress, expanding or increasing the number of blood progenitor cells. High levels of ROS were found to be valuable in this context.
A new FRET-based sensor has been developed for real-time imaging of intracellular redox dynamics, allowing for the quantification of redox state. The sensor's dynamic range is improved, enabling better discrimination between redox states in complex biological specimens.
Ruhul Abid's groundbreaking research reveals that reactive oxygen species (ROS) play a beneficial role in activating eNOS and maintaining coronary vasodilation, challenging the long-held notion of ROS being harmful. The discovery has potential implications for the development of therapeutic modalities for vascular diseases.
Researchers found that eliminating the gene for cyclophilin A from mice prevented the development of abdominal aortic aneurysm and atherosclerosis. The study suggests that targeting cyclophilin A could potentially address both conditions, which are linked by shared biochemical pathways.