Articles tagged with Lysosomal Function
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A new study has created a comprehensive atlas of lysosomal proteins in the brain, shedding light on the functions and dysfunctions of these cellular components. The data, which includes 790 proteins associated with lysosomes, could help scientists better understand neurodegenerative diseases such as Alzheimer's and Parkinson's.
Researchers at Umea University have identified two autophagy protein complexes as the long-sought sensors of lysosomal damage. These proteins respond to protons or calcium leakage, initiating the repair system that seals the hole, thereby preventing inflammation and cell death.
Macrophage lysosomes regulate reactive oxygen and nitrogen species production, with pH influencing the balance between killing microbes and avoiding self-harm. The study provides insights into immune regulation using nanoelectrochemical sensors.
Autophagy and lysosomal pathways orchestrate the unconventional secretion of PARK7, a PD-associated protein, in response to cellular stress. The study reveals a unique mechanism involving coordinated actions of macroautophagy and chaperone-mediated autophagy.
Researchers have uncovered the molecular mechanism of ATG-9 in regulating lysosome integrity by modulating phospholipid distribution. This study suggests that reduced ATG-9 scramblase activity facilitates lysosome biogenesis and repair, highlighting ATG-9 as a promising therapeutic target for diseases related to lysosomal dysfunction.
A new study from NUS Medicine has found that the protein Spns1 plays a key role in recycling fats out of cell compartments called lysosomes, preventing diseases like lysosomal storage disorders. The research uses cryoelectron microscopy to understand how Spns1 transports fats and highlights its importance for cellular health.
Researchers uncovered how mutated PSEN2 accelerates disease progression in familial Alzheimer's disease by impairing synaptic function and disrupting cellular processes.
A Pitt study found that protein STING plays a protective role in cellular stress clearance and cell survival, increasing autophagy and lysosome production. The findings suggest targeting inflammation pathway downstream of STING may be a better approach to develop therapeutics for age-related diseases.
Inflammation in immune cells, specifically macrophages, may contribute to severe symptoms in children with lysosomal storage diseases. The study suggests that blocking sodium channels or MCP-1 receptors could reduce inflammation and tissue damage.
A new study found that genetic variants in lysosomal genes may contribute to the development of Parkinson's disease in individuals exposed to high levels of pesticides. The research suggests a potential gene-environment interaction, where minor changes in these genes can lead to increased disease risk under stress.
A study published in PNAS reveals that HKDC1 protein plays a crucial role in maintaining mitochondrial and lysosomal function, thereby preventing cellular senescence. The researchers found that HKDC1 helps regulate the removal of damaged mitochondria through mitophagy and facilitates lysosomal repair.
Researchers at Tokyo Medical and Dental University have developed a novel method to characterize protein-binding interfaces, revealing complex protein geometries. The technique was validated by studying the homophilic interaction between LAMP2A molecules, which form a trimeric structure in mammalian cells.
Mutations in parkin gene break down contacts between lysosomes and mitochondria, disrupting essential metabolite supply to mitochondria. Restoring these contacts may represent a new therapeutic opportunity for Parkinson’s disease.
Researchers developed a new probe to measure pH levels in cells, revealing a constant conversion rate from endosomes to lysosomes. The probe's ability to track pH changes enables faster diagnosis and potential treatments for lysosomal diseases.
A research team led by the University of Cincinnati's Atsuo Sasaki aims to understand how an enzyme regulates lysosomal function based on energy molecule GTP. This study could lead to new treatments for cancer, neurodegenerative diseases and anti-aging.
A fetus with infantile-onset Pompe disease has been successfully treated in utero using enzyme replacement therapy, resulting in normal cardiac and motor function. The child is now thriving as a toddler, meeting developmental milestones after receiving postnatal enzyme therapy at a pediatric hospital.
Researchers at Duke-NUS Medical School have identified a protein called Spns1 that transports broken-down phospholipids out of lysosomes and into the cytoplasm, where they can be recycled. This finding further understanding of the role of lysosomes in lipid metabolism and disease, particularly in rare genetic disorders.
Researchers from NYITCOM are using a new imaging technique to study diabetic heart failure and its causes. They hope to develop new treatments by tracing how lysosomes, the body's defense system, are impaired in heart muscle cells.
Researchers at University of Cincinnati develop a new probe and imaging technique to study lysosomes, aiding in cancer and neurodegenerative disease research. The probe, known as EC Green, enables multidimensional analysis of lysosome dynamics and provides stable tracking capabilities.
A mutation in the CLCN6 gene has been identified as a cause of a novel, severe neurodegenerative disease affecting three unrelated children. The condition is characterized by developmental delay, intellectual disability, and progressive brain atrophy.
Researchers at Baylor College of Medicine identified ceramides as key players in the development of early onset Parkinsonism. The findings propose a mechanism connecting previously identified cellular defects and genes associated with Parkinson's disease, suggesting novel strategies to prevent or treat the condition.
Researchers discover progranulin's novel function as a chaperone for lysosomal protease cathepsin D, contributing to neuronal dysfunction in FTD. Progranulin knockout mice show impaired axonal regeneration after nerve injury, highlighting its importance in neurotrophic support.
Researchers at DGIST have identified a mechanism to reverse cellular aging and promote recovery through the inhibition of ATM protein. By activating lysosomal functions, they were able to restore cell division capacity and induce wound healing in aging animal models.
A Scripps Research Institute team has discovered a mechanism to enhance the cellular folding and function of mutated lysosomal enzymes, which are linked to Gaucher's disease. The researchers used FDA-approved drugs to increase calcium levels in cells from patients with Gaucher's disease, potentially paving the way for clinical trials.
Researchers identified a platelet-regulating gene mutation involved in lupus nephritis, and a novel adhesion molecule implicated in rheumatoid arthritis. The study suggests links between the mutations, loss of protein expression, defect in platelet function, and regression of kidney damage.