Articles tagged with Glutamine
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Researchers discovered that high levels of protein BATF2 drive tumor immune suppression in head and neck cancer. Glutamine in the tumor microenvironment silences BATF2, affecting the STING signaling pathway and overall immune response.
Researchers discovered that short-term physical activity decreases liver disease severity by breaking down branched-chain amino acids in skeletal muscle. This process enhances redox balance and inhibits lipid accumulation in hepatocytes.
Researchers at Sanford Burnham Prebys found that pancreatic cancer cells rely on a specific nutrient, glutamine, to fuel their unchecked growth. The study identified two enzymes, aPKC zeta and iota, that play a regulatory role in the process of macropinocytosis, allowing cancer cells to scavenge alternative resources.
Researchers at St. Jude Children's Research Hospital identified a key role for glutamine in red blood cell development and disease. Glutamine metabolism plays a critical role in removing toxic byproducts, such as ammonium, that can accumulate during heme production.
A study by Ohio State University researchers found that combining pimozide with CB-839 can effectively suppress glioblastoma growth by blocking lipid production and starvation of tumor cells. This innovative combination may also hold promise for treating other cancers relying on glutamine and lipids.
Researchers propose a two-pronged attack on the enzyme glutaminase and protein HuR to combat breast cancer. Simultaneous inhibition of both is shown to significantly reduce breast cancer cell growth and invasion by increasing dependence on glutamine.
A groundbreaking study reveals how TRMT10A deficiency disrupts protein synthesis, synaptic structure, and function in the brain, leading to impaired cognitive abilities. Researchers found a significant decrease in specific tRNA levels, particularly those essential for initiating protein synthesis.
Researchers at Cold Spring Harbor Laboratory have discovered a strategy to kill breast cancer cells and shrink tumors by depriving them of two vital nutrients: glutamine and its backup supply, alpha-ketoglutarate. This approach was successful in lab experiments and effective in treating tumors in mice.
Researchers have identified a rare genetic condition, Glutamine Synthetase Stabilization Disorder, which causes seizures and delayed development. The study found that genetic variants increase the stability of an enzyme producing glutamine, disrupting brain development.
Scientists discovered how methanogenic archaea regulate nitrogen uptake using a molecular switch that adjusts enzyme activity based on 2-oxoglutarate levels. This regulation prevents energy waste when cells have enough nitrogen.
Researchers discuss reductive carboxylation of glutamine as a potential target in acute myeloid leukemia (AML), an aggressive cancer with poor patient outcomes. The approach aims to weaken tumor cell survival mechanisms, potentially leading to novel therapies and improved patient outcomes.
Researchers at Johns Hopkins Medicine discovered a promising experimental drug combination that reduces the size of peripheral nerve sheath tumors in mice and increases survival rates. The combination blocks glutamine metabolism and purine recycling, producing a better anti-tumor response with less toxicity.
Glutamine metabolism plays a crucial role in cancer cell growth and survival, with its inhibition shown to block cancer cell growth in vivo and in vitro. A recent editorial paper suggests that glutamine dysregulation may also impact the tumor microenvironment, potentially leading to increased oxidative stress and cancer cell death.
St. Jude researchers found that supplying glutamine to tumors enhances the immune system's cancer-killing activity, while a molecular pathway identified as a potential drug target could improve anti-cancer therapies. Glutamine helps activate dendritic cells, which then activate T cells that kill cancer cells.
Researchers discovered that FDA-approved HDAC-inhibitors can impact energy metabolism in solid tumor cells, including glioblastoma. The combination of HDAC-inhibitors and imipridones may synergize to enhance killing of GBM cells by reversing cellular respiration.
Researchers discovered polyphenol PCB2DG reduces inflammatory responses by inhibiting glutamine uptake in CD4+ T cells, promoting gene expression to synthesize amino acids. The study's findings offer potential for dietary polyphenol treatment of autoimmune diseases.
A new prodrug called DRP-104 targets cancer cells' high demand for glutamine, eliminating them while sparing healthy tissues. The drug is in early-stage clinical trials for advanced solid tumors and shows promise as a safer alternative to existing treatments.
Researchers discovered that zinc can restore the functioning of proteins affected by mutations in the GNAO1 gene, leading to severe mental and motor disabilities. By reactivating hydrolysis, zinc enables neurons to communicate correctly with their environment.
Researchers found that a diet rich in butyrate sharply reduced the risk of biliary atresia in mouse pups, and identified glutamine as a key compound with similar protective effects. The findings suggest a potential role for maternal microbiome manipulation in preventing liver disease.
Researchers at Duke University Medical Center identified a key reason hormone therapies fail and proposed a new treatment strategy directly targeting the cancer's fuel source, glutamine. By inhibiting glutamine utilization, tumor growth is successfully inhibited in studies using prostate cancer cell lines and animal models.
Researchers have identified a small molecule drug candidate that targets the uptake of glutamine in cancer cells, slowing the growth of melanoma and other cancers. The study, published in Molecular Cancer Therapeutics, offers an exciting new therapeutic approach for treating tumors addicted to glutamine.
Mutations in the ARID1A gene increase glutamine metabolism in ovarian cancer cells, which can be blocked to target ARID1A-mutant tumors. Glutaminase inhibitors like CB-839 show promise as a standalone or combination therapy for clear cell ovarian carcinoma.
Chlamydia bacteria reprogram human host cell metabolism to increase glutamine import, essential for proliferation. The discovery could lead to new treatments for chronic infections and severe diseases like cervical and ovarian cancer.
Researchers found that the influenza NS1 protein can bind to the cell's RIG-I protein, quelling the alarm that activates the cellular innate immunity defense against infection. This newly described mechanism increases viral survival and highlights the need for better vaccines and antivirals.
Researchers break down amino acid glutamine when bombarded with different doses of electrons. This process has implications for understanding the effect of ionising radiation on human cells and improving cancer radiotherapy.
A new study suggests that glutamine supplementation could help people with obesity reduce inflammation of fat tissue and reduce fat mass. Glutamine levels were found to alter gene expression in several different cell types, leading to anti-inflammatory effects on white blood cells and T-cells.
A compound developed by Johns Hopkins researchers has been shown to slow tumor growth, alter the tumor microenvironment, and promote durable and highly active anti-tumor T cells. The drug, a prodrug version of glutamine antagonist DON, was designed to target cancer cells' high demand for glutamine.
Researchers at the University of Groningen elucidated the human ASCT2 structure, providing unprecedented insight into its workings and potential as a target for new anti-cancer drugs. The 'one-gate elevator' mechanism reveals a surprising similarity in release and catch mechanisms on either side of the cell membrane.
Researchers paired a calorie-restricted ketogenic diet with a tumor-inhibiting antibiotic to destroy cancer stem cells and mesenchymal cells in glioblastoma, a fast-moving brain cancer. The combination killed tumor cells while reversing disease symptoms and improving mouse survival.
Researchers have identified a genetic variant influencing the age of onset in Huntington disease, beyond just the length of the expansion mutation. This new predictor may enable families with additional information and improve disease management by providing genetic counsellors with valuable data.
Researchers at University of Pennsylvania have developed new diagnostic tools to measure PARP-1 and glutamine levels in breast cancers. These biomarkers can help identify patients most likely to benefit from targeted therapies, offering a non-invasive way to guide treatment.
Researchers discovered that a drug inhibiting glutamine metabolism improves certain immune cells' function while suppressing others. Inhibiting glutaminase activity protects against inflammation and disease in mouse models of various conditions.
A new study found a hitherto unknown error in the transport of glutamine between astrocytes and neurons in mice with Huntington's disease. The researchers believe this area holds potential for developing a future treatment.
Researchers found that glutamine is not a primary fuel for NK cells, but rather glucose. This discovery has significant implications for cancer therapies under development by pharmaceutical companies.
Researchers at University of Groningen have elucidated the 3D structure of ASCT2, an amino acid transporter involved in various cancers. The study provides new insights into the protein's mechanism and potential targets for drug development.
Researchers at Osaka University discovered that Pib2 interacts with the TOR complex to detect glutamine levels, regulating cell growth and autophagy. The study found that glutamine binding activates the TOR complex, leading to controlled cellular responses.
Researchers at Western University found that female rugby players experience brain changes during the regular season comparable to those caused by concussions, with glutamine levels reduced and potential implications for recovery. The study's authors suggest these metrics may be more sensitive to brain injury.
Researchers have discovered a long-sought source of ocean methane, a potent greenhouse gas contributing to global warming. The enzyme methylphosphonate synthase (MPnS) is found in abundant marine microbes and may produce the compound that is converted to methane.
Researchers at Penn are building a positron emission tomography (PET) scanner that can image a patient's entire body at once, allowing them to see both glucose and glutamine on the same scan. This will enable better understanding of how these two compounds interact with cancer cells.
Scientists have identified mutations in the CARD11 gene that lead to severe atopic dermatitis, an allergic skin disease. Supplementing with the amino acid glutamine may partially correct the underlying cell-signaling defects, according to a study published in Nature Genetics.
Researchers found that tumor cells entering a reversible state of proliferation arrest when glutamine is depleted, rather than dying. c-MYC levels are down-regulated upon glutamine deprivation, suggesting it couples transcription to nucleotide availability.
A study by Osaka University reveals that colorectal cancer cells can survive under glucose-depletion conditions by maintaining TCA cycle activity and ATP production. Key proteins GLUD1 and SLC25A13 play pivotal roles in nutritional stress and are associated with tumor aggressiveness.
Researchers have discovered a technique to improve the function of engineered organs and tissues by starving stem cells of glutamine, leading to more mature and functional endothelial cells. This method may prove useful for tissue engineering, particularly in the creation of functional blood vessels from human embryonic stem cells.
Researchers block glutamine breakdown in liver cancer cells, preserving normal cells, and reduce tumor development in mice. The study identifies LRH-1 as the key protein involved and suggests it as a new target for treating liver cancer.
Researchers at IRB Barcelona have identified a molecular system of protection that involves the androgen receptor protein in Kennedy's disease. The study suggests that targeting specific regions of the protein may lead to new therapeutic targets for the condition.
Researchers identified a vital supply route for cancer cells to obtain nutrients, blocking this pathway led to significant tumor growth reduction. The discovery offers new hope for developing targeted treatments with fewer side effects.
Researchers at Sandia National Laboratories and the University of Maryland have developed a new cancer treatment method that withholds an essential nutrient from cancer cells, starving them until they self-destruct. The method involves removing asparagine, a nutrient that cancer cells can't produce on their own.
Glioblastoma's aggressive nature is fueled by mTOR-induced pathways, but mTOR inhibitors have shown limited effectiveness. Compensatory glutamine metabolism plays a crucial role in mTOR inhibitor resistance, as evidenced by increased glutaminase and glutamine levels in GBM cells and tumor xenografts.
A study by Sanford-Burnham Medical Research Institute identifies a protein called RNF5 that determines breast cancer response to paclitaxel, a chemotherapy drug. The researchers found that RNF5 causes degradation of glutamine carrier proteins, leading to sensitization of breast cancer tumors to death.
A study found that high-protein enteral nutrition enriched with immune-modulating nutrients does not reduce new infections or improve outcomes in critically ill patients. In fact, it may be harmful, increasing the risk of death at 6 months.
Research published in the Journal of Parenteral and Enteral Nutrition found that patients who received glutamine supplements had a significantly higher mortality rate than those who did not. The study involved over 1,200 patients across 40 ICUs in North America and Europe.
Researchers at Ohio State University Comprehensive Cancer Center identified a molecular pathway that enables cancer cells to grow in low-oxygen environments. By targeting this pathway, therapeutic strategies may be developed to inhibit tumor growth with minimal side effects.
Researchers found that protein aggregation has beneficial functions allowing cells to organize themselves in time and space. Protein aggregation helps create spatial patterns in transcripts, influencing protein localization and function.
Researchers found a small piece of RNA that blocks glutamine production in the colon, leading to diarrhea, bloating, and abdominal pain. Silencing this RNA segment may open up a new approach to treating IBS symptoms.
Researchers at Huntsman Cancer Institute have discovered that restricting glutamine availability can halt tumor growth by blocking glucose utilization. This breakthrough could lead to the development of new drugs targeting glutamine utilization or MondoA/ TXNIP.
Researchers found that glutamine supplementation can lower inflammation in stomach tissue infected with H. pylori bacteria, a primary cause of stomach cancer. The study suggests a potential new treatment option for stomach ulcers and gastric cancers.
Scientists at the Weizmann Institute have proposed a mechanism that explains the precision of trinucleotide repeat diseases like Huntington's. They suggest that the genes carrying the disease code accumulate more DNA repeats over time until a critical threshold is crossed.
Researchers discovered that abnormal glutamine repeats interfere with key transcription factor TBP, leading to neurodegeneration in PolyQ diseases. The study provides insight into the molecular mechanisms underlying these inherited disorders.
Researchers found that abnormally long glutamine tracts in proteins can cause nerve cells to deteriorate and die. The study suggests that understanding the molecular mechanism behind polyglutamine diseases may lead to the development of new treatments, including small molecule drugs.
Spinocerebellar ataxia type 1 (SCA1) is caused by a toxic buildup of the protein Ataxin-1, leading to damage in cerebellar Purkinje cells. Researchers discovered that glutamine repeats in the protein cause toxicity, which can also affect other neurodegenerative diseases like Huntington's and Parkinson's.