Articles tagged with Autophagy
Research finds autophagy rates don't decline with age as expected, but rather vary in different cell types and are influenced by sex. Exercise may modify autophagy levels in humans, potentially reducing blood cell activity in older adults while improving physical performance.
Researchers have identified GW406108X, a broad-spectrum antiviral compound, that can inhibit a range of enteroviruses, including EV-D68, by targeting a process in human cells. The compound showed activity against multiple viruses, including Rhinovirus A16, and reduced EV-D68 levels by 1,000-fold in laboratory experiments.
Researchers have discovered the underlying mechanism of Atg2-mediated lipid transfer in autophagy, revealing two distinct mechanisms that enable proper growth of the autophagosomal membrane. The phosphorylation of a specific region of Atg2, mediated by Atg1, enables its binding to the endoplasmic reticulum and subsequent lipid transfer.
Researchers found that enhancing autophagy, a cellular recycling process, helps preserve retinal nerve cells in glaucoma models. This approach may protect against cell loss and degeneration, potentially complementing current treatments.
New study reveals how resistance exercise damages skeletal muscle and triggers a coordinated repair process. The research identifies key proteins involved in this network, providing insights into optimizing training programs for athletes and improving rehabilitation strategies.
Research identifies SPP1+ macrophages as key drivers of intervertebral disc degeneration, leading to matrix destruction and disc deterioration. Targeting the SPP1 signaling pathway may offer an effective strategy for mitigating or reversing spinal degeneration.
Researchers have developed an innovative combination treatment strategy that uses cells' waste removal functions to effectively dismantle multiple myeloma. The experimental targeted protein degrader enhances the destruction of a specific cancer cell survival protein and works in tandem with existing drugs, while showing limited toxicity.
Researchers at Olivia Newton-John Cancer Research Institute discovered that reduced BECLIN1 levels weaken the gut's protective barrier, leading to increased susceptibility to inflammation and disease. This finding may help explain why some people are more susceptible to gut inflammation and associated diseases.
Researchers identified two parallel neuronal circuits regulating autophagy-lysosome pathway in C. elegans body wall muscle. The first circuit involves electrical synapses and the second originates from ASI sensory neurons, both converging on a Ca2+-calpain-lysosome signaling cascade to maintain muscle homeostasis.
A team from the University of Osaka has created a high-throughput platform to engineer versatile biosensors that can track lipid molecules in living cells. This method, called Cell surface Liposome Binding (CLiB) assay, uses yeast cells and fluorescence readouts to test protein variants' binding to lipids.
Prostate cancer cells use the PIM1 protein to survive treatment by activating autophagy, a cellular recycling process. Researchers have discovered a potential strategy to overcome this resistance by removing the PIM1 protein entirely using a proteolysis-targeting chimera.
Researchers suggest targeting upstream metabolic nodes to regulate mTORC1 signaling and autophagy defects in neurodegenerative diseases. Acetyl-CoA production modulation and p300 acetylation activity regulation may also hold therapeutic promise.
GLP-1 RAs improve mitochondrial function, reduce oxidative stress, enhance autophagy, and attenuate inflammaging. They affect all 12 hallmarks of aging, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, insulin resistance, and dysbiosis.
A team of researchers has identified a key mechanism in the degeneration of motor neurons in ALS, revealing that chaperone-mediated autophagy is significantly reduced in patients. This finding suggests that this cellular system may be a potential therapeutic target to slow disease progression.
Researchers found that a novel compound can clear harmful protein from human neurons modeling frontotemporal dementia, preventing neuron death. Enhancing autophagy with the compound showed promise as a treatment strategy for neurodegenerative diseases.
A study published in eGastroenterology reveals that Autophagy Related 14 (ATG14) plays a critical role in protecting the liver against injury and fibrosis. ATG14 deficiency leads to severe hepatocellular injury, oxidative stress, and inflammation, highlighting its importance in maintaining hepatocyte homeostasis.
A new study shows that pancreatic cancer cells' ability to detect the extracellular matrix determines their growth rate and response to chemotherapy. The researchers found that cells detecting ECM have low autophagy levels and high growth rates, while those farther away from ECM have high autophagy levels and can survive chemotherapy.
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 research team at Goethe University Frankfurt has compiled a catalog of human E3 ligases and mapped their relationships, revealing family-specific functions. The study identifies 40 additional E3 ligases suitable for PROTAC development, expanding the range of tissues and diseases targeted by degradation therapies.
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.
Researchers found that a decline in chaperone-mediated autophagy activity is linked to age-related muscle wasting and can be boosted by exercise and fasting. The study suggests that enhancing this process may be a promising therapeutic strategy for preventing or treating sarcopenia in aging populations.
Researchers discovered that brain enzyme OTULIN regulates tau protein accumulation and has implications for treating neurodegenerative diseases. The study revealed OTULIN's role in controlling gene expression and RNA metabolism, suggesting a potential therapeutic target.
Researchers found that vitamin D receptor deficiency disrupts autophagy and promotes epithelial-mesenchymal transition, leading to endometrial fibrosis. Vitamin D or VDR-targeted therapy may serve as a promising approach for preventing or treating intrauterine adhesion.
A new study reveals that combining proteasome inhibitors with Lys05 can effectively kill AML cells by disabling backup survival pathways. This approach has shown promise in preclinical models and could lead to improved treatment options for a wider range of AML patients.
A recent study reveals that circFKBP8(5S,6) or cFKBP8 promote susceptibility to chronic unpredictable mild stress in mice by down-regulating DRD3 expression and disrupting AMPK/mTOR/ULK1 autophagy signaling. Behavioral studies demonstrate exacerbated depressive-like phenotypes, which can be mitigated by the DRD3 agonist cariprazine.
A new study from Aarhus University reveals how cells slice built-up protein clumps into manageable pieces to eliminate waste. Researchers discovered a key mechanism involving the proteasomal 19S subunit, which could lead to enhanced autophagy and improved treatments for neurodegenerative diseases.
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.
A team of researchers from Aarhus University has identified the molecular 'switch' regulating autophagy, a process by which cells recycle unwanted materials. The discovery could lead to new treatments for diseases such as cancer, neurodegeneration, and infection.
Damage to the intestinal barrier is a key factor in IBD pathogenesis. The barrier maintains homeostasis by preventing harmful substances from entering systemic circulation. Emerging therapeutic strategies target oxidative stress modulation, microbiota restoration, and autophagy regulation.
The Zika virus employs its host cells' autophagy mechanism to suppress proteins that would trigger an antiviral response, allowing for sustained infection. This unique strategy involves the manipulation of three proteins on the viral membrane, which are also involved in viral entry and replication.
Scientists have discovered a mechanism that controls tomato ripening, regulated by autophagy, which also affects life- and health-span in humans and animals. This finding has significant implications for reducing food waste and addressing sustainable food security.
Researchers investigated why bones become less responsive to exercise with age, finding increased mtROS or decreased Atg7-dependent autophagy in osteoblastic cells do not contribute to reduced mechanoresponsiveness. Damage to the bone's osteocyte network also does not prevent a healthy bone-building response.
A new study found that repeated cold exposure improves autophagic function in young males, enhancing cellular health and increasing cellular cold tolerance. This research provides scientific backing for the potential health benefits of cold water immersion and suggests its potential to prevent diseases and slow down aging.
Compound K exhibits anti-aging properties by enhancing skin barrier function, preventing photoaging, and regulating autophagy. It also protects against mitochondrial dysfunction and promotes tight junctions between keratinocytes.
A recent study found that autophagy, a natural defense mechanism in cells, is less efficient in female eggs with moderate or severe DNA damage. Boosting autophagy can improve egg quality and reduce the risk of miscarriage and birth defects. The study's findings offer new directions for improving reproductive health.
Researchers identified two venom genes in parasitoid wasps that degrade adult tissue precursors in host fly larvae, ensuring successful parasitism. The findings provide insights into the molecular mechanisms behind the sophisticated survival strategy of these wasps.
A novel patient-derived organoid library of tongue cancer tissue samples reveals new insights into chemoresistance mechanisms, highlighting the importance of autophagy and cholesterol biosynthesis pathways. The research also identifies potential drug targets for overcoming chemotherapy resistance in tongue cancer.
Macronucleophagy helps maintain cell viability in nitrogen-starved yeast by modulating micronucleophagy. Uncontrolled micronucleophagy causes cell death, but a critical role for macronucleophagy was found to prevent this.
Researchers have discovered a mechanism to detach and recycle parts of cellular canal membranes as needed. The study, conducted with supercomputer simulations, shows that protein regions can cause the membrane to bulge and pinch off, forming vesicles for recycling.
A new study by MUSC researchers reveals how cancer cells develop resistance to hydroxychloroquine, an anti-malarial drug repurposed for cancer therapy. The findings suggest that targeting specific metabolic and export pathways can prevent resistance, opening the door for novel combination therapies.
Scientists have found that biomolecular condensates can cross membranes without specialized cutting proteins, a process called wetting, which is essential for plant survival. The study shows that these liquid droplets can exert large capillary forces on membranes, cutting them in two and enabling material exchange between cell parts.
Chung-Ang University researchers have identified a potential anti-aging drug called IU1 that enhances proteasomal activity and autophagy, leading to improved muscle strength and extended lifespan in fruit flies. The study suggests that preventing disruption of protein homeostasis mechanisms could be key to increasing longevity and impr...
A research team led by Osaka University has identified a new mechanism crucial for the initiation of autophagy, a self-degradation process cells use to eliminate unneeded or damaged components. The palmitoylation of ULK1 by ZDHHC13 plays a critical role in this process.
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 NTU Singapore and Oxford have identified a new process called nucleophagy that helps cells remove harmful DNA-protein lesions, promoting genetic material stability and cell survival. This discovery may improve cancer treatment outcomes for patients with colorectal cancer.
A University of Bonn study reveals that strength training activates the BAG3 system, essential for eliminating damaged cell components. This finding holds promise for new therapies for heart failure, nerve diseases, and even benefits for manned space missions.
A recent study at Rice University found that using synthetic data to train generative AI models can lead to negative consequences, including model collapse and reduced quality. As models become increasingly dependent on self-consuming loops, they may produce warped outputs lacking diversity or quality.
Researchers found that GZ17-6.02 killed uveal melanoma cells by enhancing autophagy, inactivating key proteins, and reducing growth factors. The compound also interacted with doxorubicin and ERBB inhibitors to enhance tumor cell killing, suggesting potential as a single agent or combination therapy.
Researchers from the University of Copenhagen discovered that a biological mechanism called autophagy plays a key role in plant root growth. By understanding how plants control their root growth, scientists can develop climate-resilient crops to thrive in harsh conditions.
The study reveals that ALS-linked C9orf72 dipeptide repeats inhibit starvation-induced autophagy by modulating the interaction between BCL2 and BECN1/Beclin 1. This inhibition impairs autophagic clearance of neurodegenerative disease-associated protein aggregates under starvation conditions.
Researchers at Goethe University Frankfurt have discovered thalidomide derivatives that target and degrade BCL-2, a protein essential for the survival of cancer cells. The derivatives bind to CRBN, reprogramming its binding surface to mark BCL-2 for degradation, ultimately leading to cell death.
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 reveals that increased levels of TP53INP2 correlate with greater muscular strength and healthier ageing in humans. Boosting this protein's presence improves muscle mass and function, suggesting a potential strategy to combat sarcopenia.
Depletion of axonal mitochondria disrupts autophagy, leading to abnormal protein build-up in neurons. Restoring mitochondrial levels restores autophagy and recovers impaired neuron function.
Cells use autophagy as a recycling system to transport and break down damaged organelles, including mitochondria. A recent study reveals the molecular details of how an enzyme called TBK1 participates in mitophagy, a disease-relevant process linked to Parkinson's disease.
Researchers discovered GZ17-6.02's ability to interact with proteasome inhibitors in a greater than additive fashion to kill multiple myeloma cells and alone inhibit inhibitor-resistant cells. The compound combination also activated key pathways and increased autophagosome formation, leading to tumor cell killing.
Researchers at UC Davis identified a promising new fungicide, ebselen, that targets the autophagy pathway to prevent fungal infections in crops. The chemical has shown anti-inflammatory and neuroprotective properties in humans and is more effective than currently available fungicides.
Researchers found GZ17-6.02 alone and in combination with standard-of-care agents was effective in killing MF cells, activating key pathways including ATM, AMPK, NFκB, and macroautophagy. The compound's unique multi-factorial mechanism suggests potential for treating mycosis fungoides.
A team of researchers from Nara Institute of Science and Technology discovered a phytohormone-mediated switch controlling autophagy, leading to terminal cell differentiation for petal abscission. They found that jasmonic acid promotes petal abscission by activating autophagy at the base of petals.
Researchers developed a new photosensitizer, polphylipoprotein (PLP), to improve photodynamic therapy (PDT) efficacy. PLP selectively induces necrosis in cancer cells by exploiting the autophagy mechanism under starvation, leading to high selectivity and potential efficacy.