Articles tagged with Receptor Activation
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Scientists at Virginia Tech uncover how abscisic acid, a natural plant hormone, fights inflammation by interacting with the lanthionine synthetase C-like 2 protein. This alternative mechanism avoids known adverse side effects of existing drugs, paving the way for new treatments.
B-cell receptors form ordered oligomer complexes that only become active when binding partners disintegrate into subunits. This new model challenges the accepted scientific doctrine and may contribute to the development of new vaccination strategies and treatments for B-cell tumours.
Researchers at Max Planck Institute discover that flushing phenomenon triggered by nicotinic acid is caused by activation of Langerhans cells and keratinocytes, leading to inflammation and skin redness. Development of novel 'flush inhibitors' could improve treatment outcomes for cardiovascular diseases.
Researchers at Duke University have found a new mechanism of bone formation that works without inducing bone breakdown, suggesting a targeted approach to fighting osteoporosis and other degenerative bone diseases. The discovery involves the G-protein coupled receptor (GPCR) pathway and beta-arrestin molecule.
The study identified the B1-receptor as a key player in regulating T cell entry into the central nervous system. Activation of this receptor slows down T cell entry and reduces clinical symptoms of inflammation in multiple sclerosis, suggesting a potential new target for therapy.
A new study from the University of Cincinnati finds that cigarette smoke can activate specific immune system receptors, leading to worsening of chronic obstructive pulmonary disorder (COPD) symptoms. The research identified a key cellular receptor, NKG2D, involved in this process.
A study by the University of South Florida Health Sciences Center found that resveratrol reduces fat production and increases breakdown in the liver of mice fed alcohol. This prevents accumulation of fat and suggests resveratrol as a promising agent for preventing or treating human alcoholic fatty liver disease.
A study published in PLOS Biology reveals the molecular structure of COUP-TFII, a nuclear receptor regulating gene expression in cells. The findings suggest potential drug targets for diseases related to heart development, human embryonic development and female infertility.
Researchers at UC San Diego School of Medicine have uncovered a new signaling mechanism used to activate protein kinases involved in the body's inflammatory response. Smac mimic compounds may serve as prototypes for new anti-inflammatory therapy, potentially offering an alternative to expensive current treatments.
A new study using rats found that THC combined with mildly intoxicating doses of alcohol induced widespread nerve cell death in the brain. The study also showed that THC enhanced the neurotoxic effect of other substances, including phenobarbital and MK-801.
Researchers identify the first protein to activate G-protein signaling from within a cell, opening up new pathways for drug development. The discovery of Arr4 could lead to more selective and effective medications with fewer side effects.
Researchers at the Salk Institute have discovered a molecular pathway that regulates immune inflammation, known as the TAM receptor tyrosine kinase. The study found that activating this pathway can help control chronic autoimmune diseases such as lupus and rheumatoid arthritis by inhibiting an out-of-control inflammatory response.
A new study finds that the TRPM8 ion channel plays a crucial role in detecting cold temperatures by activating neural impulses. The research suggests that TRPM8 is not the sole receptor responsible for detecting extreme cold, indicating possible alternative pathways.
Researchers found that cocaine affects dopamine and glutamate receptors, interfering with normal activation of glutamate receptors. This interaction between D2R and NR2B subunits is critical for mediating cocaine's effect on motor responses.
Researchers at UCSD School of Medicine have reconstructed the signaling pathways that regulate activation of glycoprotein IIb-IIIa, a critical receptor in platelet function. The study provides a powerful tool for studying therapeutic targets and developing new antithrombotic drugs.
A team of neuroscientists has identified a specific molecular mechanism that targets the machinery causing fusion process, allowing for controlled release of neurotransmitters instead of an all-or-none release. This discovery has important implications for treating neurological conditions and may lead to new drugs.
Researchers at UNC have identified CIB1 as a 'gatekeeper' protein that inhibits platelet-to-platelet interactions in the blood. By binding to GPIIb/IIIa, CIB1 prevents platelet activation and clot formation.
Researchers discovered that nicotinic acid activates GPR109A on fat cells to lower lipid levels, but on immune cells in the skin, it triggers flushing responses. This study supports the hypothesis that immune cells are a primary source of arachidonic acid and prostaglandins causing hot flashes.
Researchers develop a computer model simulating signal transmission at a synapse in chick embryos, finding that 90% of neurotransmitter release occurs outside of synapses. This discovery opens up new possibilities for cell-to-cell communication in the nervous system and challenges traditional definitions of synapses.
Researchers have identified a molecular mechanism controlling lung dryness and fluid entry, potentially leading to better prognosis for those with acute respiratory distress syndrome. The discovery focuses on the SIP3 receptor, which, when activated, causes pulmonary edema, offering new avenues for treatment.
Researchers engineered a decoy Met receptor that successfully competes for HGF binding, inhibiting tumor growth and survival. The Sema domain of the Met receptor is also necessary for activation, offering a new therapeutic target for cancer treatment.
Researchers have found that the lack of response occurs because IGF-I does not activate its receptor molecule on the surface of the cells, triggering a signaling feedback loop. Integrins, which regulate growth factors in other cells, are also impaired due to skeletal unloading.
Activation of the PPAR-delta receptor increases development of precancerous intestinal polyps in mice, with larger polyps being more likely to progress to colorectal cancer. Treatment with a specific compound linked to the receptor may accelerate polyp growth through antiapoptotic pathways.
NF-kappaB plays a complex role in atherosclerosis, both promoting and inhibiting inflammation. In mice deficient in LDL receptors and NF-kappaB activation, lesions were larger and more advanced, containing more necrosis and macrophages.
Researchers identified OEA, a natural fatty acid, that activates cell receptors to curb hunger and reduce weight in rodents. The study found that increasing OEA levels while maintaining normal receptor activity can lower blood cholesterol and triglyceride levels.
Researchers discover PlGF-1 stabilizes vessel growth in premature infants, preventing retinal detachment and blindness. The study suggests a promising therapeutic agent to prevent oxygen-induced vascular degeneration in ROP.
A study published in the Journal of Clinical Investigation found that HIV protease inhibitors directly promote atherosclerosis in mice. In humans, researchers propose a mechanism by which these drugs might contribute to heart disease, suggesting ways to disrupt it.
New studies suggest that vitamin D may help prevent colon cancer by activating the detoxification of lithocholic acid, a known carcinogen. Researchers found that vitamin D acts as a sensor for the toxic chemical, triggering proteins to clear it from the body.
Researchers have identified a novel mechanism for activating G-proteins without external stimulation, which supports cellular polarity in asymmetrically dividing cells. This discovery has significant implications for understanding disease mechanisms and developing novel therapies.
Researchers show that the transcription factor E2F-1 activates both p53 and p73, playing a crucial role in cell death. This finding raises the possibility of using activators of E2F-1 to tip the balance towards apoptosis, potentially leading to new cancer therapies.
Researchers at UC San Francisco found that activated pain nerve fibers dampen the inflammatory response's first line of attack, preventing chronic diseases. The study suggests that pain acts as a negative feedback control of inflammation, which can help prevent chronic inflammatory diseases.
Neurobiologists at Duke University Medical Center have captured the first detailed images of the living brain in action, revealing how it recognizes specific odor molecules. The imaging technique can provide new insights into the machinery of learning and help decipher the brain's internal 'language' of smell.
Researchers at UCSF have discovered a new molecular mechanism that activates platelets, leading to clot formation. The discovery of protease-activated receptor 4 (PAR4) may lead to new approaches for developing drugs to prevent heart attacks and strokes.
Scientists have identified SLP-76 as a critical protein for the development and activation of T cells, an essential part of the immune system. This finding provides valuable insights into the basic biology of immune system activation, which is crucial for understanding immunodeficiency disorders and autoimmune diseases.
Fetal rat skin cells treated with hormone activators formed a competent barrier earlier than control groups, reducing water loss and increasing enzyme activity. This study suggests that hormone activators could be used to promote skin growth in premature infants.
HIV scientists discovered a biochemical cascade initiated by virus envelope proteins that activate cells and increase their vulnerability to infection. The study found macrophage-tropic viruses use CD4 and CCR5 for cell entry, while T-cell tropic strains do not trigger signalling.