Articles tagged with Lysosomes
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For the first time, researchers have directly visualized how newly formed cellular organelles leave the endoplasmic reticulum and transition onto microtubule tracks inside living cells. The study reveals that the ER plays an active role in steering intracellular traffic.
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 Mount Sinai discovered a technique to renew aged blood-forming stem cells by correcting defects in lysosomes. The breakthrough revealed that restoring lysosomal slow degradation can revitalize aged stem cells and enhance their regenerative capacity. This study may help prevent age-related blood disorders and improve stem...
Janelia researchers have uncovered a complex interplay between the ER and lysosomes, with Lunapark stabilizing ER junctions and lysosomes regulating nearby translation. This finely tuned partnership links nutrient sensing and stress signaling to protein biogenesis.
Researchers at St. Jude Children's Research Hospital found that metabolism guides the activation states of regulatory T cells, which dampen inflammation. The study reveals a link between mitochondrial function and lysosome activity in controlling these immune cells.
Researchers have discovered that activating lysosome biogenesis alleviates senescence in Hutchinson-Gilford progeria syndrome. By promoting progerin clearance, this approach shows promise as a potential therapeutic avenue for HGPS and other age-related disorders.
A study by Meng Wang and her team found that histone modifications can be transferred from parent to offspring through epigenetic changes, enabling the transfer of longevity markers across generations. This mechanism has implications for understanding transgenerational effects beyond longevity.
Researchers from The University of Osaka discovered that macrophages can directly engulf and digest damaged mitochondria through a process called microautophagy. This process allows lysosome-like compartments in macrophages to take in broken cell components directly, bypassing the need for digestion.
Researchers have developed a groundbreaking method to observe lysosomes in live suspended cells—quantitatively, in 3D, and without the use of chemical labels. The technology uses holographic tomography in flow cytometry configuration (HTFC) to identify morphological and spatial lysosomal changes in models of lysosomal storage diseases.
Tetrandrine modulates autophagy by selectively removing damaged lysosomes through lysophagy while promoting new lysosome formation. This unique mechanism highlights tetrandrine's therapeutic potential for treating neurodegenerative diseases.
Research found that Atp6v0d2 deficiency can partially compensate for the loss of Mcoln1, improving fertility. The study used a double-knockout mouse model and observed normal mating behavior but reduced fertility in some mice.
Researchers from Kyushu University found that lipid peroxidation of lysosomes plays a key role in ferroptosis-mediated cell death, leading to iron leakage and membrane permeabilization. Administration of chloroquine promotes ferroptosis even in cancer cells less susceptible to the process.
Researchers develop nanoparticle-based therapy combining hydroxyl-enriched fullerenol and mTOR inhibitors to disrupt cancer cells' organelle communication system. The approach triggers a synergistic "nanomaterial + metabolic modulation" anticancer strategy, establishing a new hope for treating aggressive cancers.
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.
Researchers used CRISPR interference to examine every gene in the human genome and discovered a new set of genes contributing to Parkinson's disease risk. The study identified the Commander complex, which regulates lysosomal function and is implicated in PD risk, offering opportunities for new treatments.
A new Northwestern University study finds that NU-9 improves neuron health in animal models of Alzheimer's disease by addressing the underlying mechanisms of misfolded proteins. The drug reduces protein buildup and prevents inflammation, showing potential for treating neurodegenerative diseases.
Isowalsuranolide activates autophagy-dependent cell death by targeting TrxR1/2, leading to ROS-mediated lysosomal biogenesis and reduced cell growth. The study reveals the TrxR1/2-p53-TFEB/TFE3 axis as a key regulator of cellular homeostasis in cancer.
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 used novel fluorescent sensors to track pH and H2O2 levels inside autophagic vesicles, revealing high levels in the middle stage of autophagy. The discovery opens up new avenues for understanding autophagy in health and disease, potentially leading to new ways of treating diseases associated with impaired autophagy.
Lysosomal TRAP effectively inhibits virus infection in cell, mouse, hamster, and human lung organoid models, including SARS-CoV-2 and influenza A. It outperforms current standard treatments and is not vulnerable to viral mutations.
Researchers at McMaster University have identified a potential treatment for Sandhoff and Tay-Sachs diseases, two rare lysosomal storage disorders that cause progressive damage to nerve cells. The FDA-approved drug 4-phenylbutyric acid (4-PBA) showed significant improvements in motor function, lifespan, and healthy motor neurons.
Researchers found that lysosomal stress can disrupt normal pancreatic function, leading to impaired insulin production and glucose regulation in various diabetes types. Targeting lysosomal function may lead to new treatments for diabetes.
Researchers discovered that INPP4B drives the movement of lysosomes to the periphery of pancreatic cancer cells, releasing their contents into the extracellular space and disrupting the structural support network. This process enables the cells to migrate and invade other tissues, making it easier for the cancer to spread.
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.
Researchers at SickKids have identified a novel recycling mechanism in mitochondria that allows damaged cristae to be removed and replaced, restoring normal function. This discovery could lead to new treatments for conditions characterized by mitochondrial dysfunction.
Researchers found that artificial induction of GluCer leads to cellular senescence in DA neurons, highlighting the role of lipid aggregation in PD. The study proposes that lysosomal impairment and lipid accumulation trigger expression of a cellular senescence phenotype in vulnerable DA neurons.
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.
Researchers have developed a model to enrich sub-populations of cancer cells with high basal levels of mitophagy, promoting CSC features such as self-renewal, proliferation, and drug-resistance. This study highlights the importance of BNIP3/BNIP3L in maintaining cancer stem cell properties.
In animal models, increasing mTOR activity just slightly accelerates aging and shortens lifetime by up to 20%. This research provides clues on why obesity-related diseases worsen with age. A new model allows researchers to study the relationship between nutrient increase and organ aging.
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.
The study reveals that TM4SF19 protein inhibits a pump in lysosomes, impeding macrophage clearance of dead cells. Macrophages lacking TM4SF19 demonstrate enhanced efficacy in clearing dead adipocytes, reducing weight gain and metabolic dysfunction. The findings may open new avenues for treating obesity and related metabolic disorders.
Researchers identified a novel mechanism where APP-CTFs disrupt organellar communication, interfering with cellular homeostasis and leading to endolysosomal dysfunction. This finding suggests that preventing APP-CTF accumulation could be crucial for developing new AD treatments.
Researchers found that nutrient-starved cells divert ER exit sites to lysosomes for degradation, using a novel pathway to free up amino acids. This process involves the recruitment of molecules to direct ER exit sites to lysosomes, where they are destroyed and their components recycled.
The study reveals two distinct modes of endosomal fusion: homotypic fusion, where small vesicles fuse rapidly, and heterotypic fusion, where large vesicles absorb endosomes. Mathematical analysis and experiments suggest that actin dynamics plays a crucial role in promoting homotypic fusion.
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 have discovered the structural proof of DNA and RNA breakdown by PLD3, an enzyme linked to Alzheimer's disease. The study provides a map of the protein, which could lead to better understanding of its role in certain diseases.
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.
A recent study by Goethe University Frankfurt has identified a mechanism that could be a suitable starting point for developing novel drugs against leukemia cells. The researchers discovered that the mutated NPM1 gene variant drives pro-autophagic activity, enabling cancer cells to recycle their structures and meet their needs.
A study published in EMBO Reports reveals that microautophagy is crucial for repairing damaged lysosomes, which helps prevent cellular aging. The researchers identified key regulators of this process, including STK38 and GABARAPs, and found that their depletion increases the rate of senescent cells and shortens lifespan in C. elegans.
A recent study published in the Journal of Cell Biology has made significant progress in understanding autophagy and lipid recycling. Researchers used yeast as a model organism to identify key players in the process, including Atg15, Pep4, and Prb1, and demonstrated that Pep4 and Prb1 activate Atg15 to break down phospholipid bilayers.
Stanford researchers have discovered a pathway to break down problematic proteins, which can be harnessed to develop new treatments for diseases such as Alzheimer's and cancer. The findings also offer insights into lysosome storage disorders, rare conditions that affect babies and children.
Researchers developed three new two-photon probes that can visualize organelles in cells, enabling better understanding of cellular functions and tissue imaging. The probes are designed to detect pH levels, viscosity, and ionic species, providing more specific insights into cell viability and treatment responses.
Researchers developed a novel material that self-assembles into micelle structures targeting cancer cell lysosomes, specifically interacting with Cathepsin B. This leads to dysfunctional lysosomes and apoptotic death of cancer cells. The technology promises a new approach to combat drug resistance in cancer treatment.
In C. elegans, a specialized anti-aggregation mechanism is triggered in response to core protein quality control failure, promoting tissue-specific resilience to age-dependent protein aggregation. This mechanism relies on pathogen response factors and lysosomal mediated degradation.
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.
Scientists used Insilico Medicine's generative AI platform to identify actionable drug targets for cystinosis and validate them in preclinical models. The study found that hyperactive mTOR signaling drives kidney tubular cell dysfunction, making it a targetable pathway.
Researchers discovered that CLN3 is essential for lysosome biogenesis and autophagic lysosomal reformation (ALR), uncovering a novel disease mechanism in Batten disease. The loss of CLN3 impairs lysosome formation, leading to the accumulation of dysfunctional lysosomes.
A new study reveals that Salmonella uses a two-pronged approach to protect itself within the host's defense mechanisms, involving protein SopB. By altering phosphoinositide dynamics and preventing lysosome production, SopB allows the bacteria to survive inside macrophages.
A team of researchers identified the substrates targeted by alpha 2-macroglobulin for degradation. They developed a novel assay to detect its role in lysosomal degradation of extracellular proteins. This finding suggests that an array of extracellular chaperones cooperate to protect against misfolded proteins.
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.
Researchers at the University of Bonn identified unique features and novel lysosomal proteins in six different cell types, including liver cells and cancer cells. The study provides new insights into cellular waste removal machinery and its role in diseases such as Alzheimer's and Parkinson's.
Researchers explore cellular senescence's complex relationship with growth stimulation and cell cycle arrest, revealing potential anti-aging drug targets. Understanding these mechanisms is crucial for developing new treatments for age-related diseases.
Research by University of Cambridge scientists reveals that a rare genetic disorder, Gaucher disease, provides protection against TB due to an unusual fatty chemical that acts as a microbicide. The study suggests that Ashkenazi Jews, who are more susceptible to Gaucher disease, may be less likely to contract TB infection.
Researchers found a genetic alteration in the SARS-CoV-2 spike protein that redirects the virus into a storage compartment within cells, reducing its surface exposure. This change may affect the immune system's ability to identify and kill infected cells.
Researchers at Harvard Medical School have made progress in understanding the mechanism underlying a type of dementia that strikes early in life. A genetic form of frontotemporal dementia is associated with accumulation of specific lipids in the brain, which results from a protein deficiency that interferes with cell metabolism.
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.
A new method allows researchers to study the contents of lysosomes in mice, enabling them to identify molecules involved in diseases such as Batten disease. By using genetically engineered mice with a molecular tag, scientists can selectively collect and analyze lysosomes, providing valuable insights into the causes of these diseases.
A new study reveals that aggregates of the protein alpha-synuclein spread in the brains of people with Parkinson's disease through a cellular waste-ejection process called lysosomal exocytosis. This process can lead to the deaths of neurons and ultimately result in the characteristic symptoms of the disease.
A team of researchers at Osaka University has identified a specific enzyme complex that initiates the removal of damaged lysosomes from cells. The complex, composed of CUL4A, DDB1, and WDFY1 proteins, acts preferentially during lysophagy to facilitate the degradation process.