Articles tagged with Proteostasis
Cells have a new fail-safe mechanism to handle misfolded proteins that accumulate in liver cells, explaining why only some patients with alpha1-antitrypsin deficiency develop liver disease. This discovery could help predict which patients are at highest risk of needing a liver transplant.
Elke Deuerling, a molecular biologist at the University of Konstanz, has been elected as a member of the Leopoldina, the German National Academy of Sciences. Her work on proteostasis, the regulation of cellular protein levels, has significantly contributed to the understanding of protein protection in delicate formation phases.
A new study reveals that impaired protein recycling is the key factor in T cell exhaustion, allowing researchers to develop a 'tag and sort' fix to restore normal proteostasis. This approach boosts the potency of cell therapy against cancer.
Researchers discover zinc levels control endoplasmic reticulum redox enzymes necessary for proper protein folding. Zinc surge disrupts oxidative folding, leading to protein misfolding and cellular defects.
A specific protein complex regulates protein balance in plants, influencing their response to environmental stress. Researchers discovered that this process, known as N-terminal acetylation, maintains the stability of the plant proteome by controlling protein degradation and recycling.
A new study reveals that blocking the aryl hydrocarbon receptor (AHR) helps neurons regrow damaged axons and recover motor and sensory function. AHR acts as a key regulator that determines how neurons respond after injury, slowing down axon growth.
Researchers discovered how VCP, an enzyme that unravels proteins, interacts with tag-removing enzymes DUBs to regulate protein degradation. This interaction may have implications for treating neurodegenerative disorders like Alzheimer's and certain cancers.
Researchers discovered a potential vulnerability in P. falciparum by inducing protein aggregation, leading to reduced parasite growth. The study may lead to novel antimalarial strategies targeting the parasite's internal protein folding machinery.
Researchers have discovered a nucleolar complex that plays a pivotal role in maintaining cellular health through protein homeostasis, allowing for the dramatic reduction of toxic effects of Alzheimer's-causing proteins. This breakthrough offers hope for new therapies to slow or prevent neurodegenerative diseases, promoting healthy aging.
A recent study reveals that the transcription factor NRF1 activates aggrephagy, a protein clearance process, in response to proteasome dysfunction. This mechanism helps maintain proteostasis and has major implications for treating degenerative diseases such as Alzheimer's, Parkinson's, and dementia with Lewy bodies.
Researchers used unbiased genetic screening to identify genes involved in regulating sleep in worms, finding that proteins play a crucial role. These findings suggest new approaches for preventing diseases related to sleep disturbances and inflammation.
Researchers identified mRNAs and long non-coding RNAs targeted by stress granule proteins, which accumulate AD-associated gene transcripts in these structures. SGs may play a key role in regulating AD development through the impairment of protein neurohomeostasis.
Researchers found that metformin + leucine (MET+LEU) treatment prevents myotube atrophy by reversing cellular senescence and improving proteostasis. The study used C2C12 myoblasts, aged mouse single myofibers, and human primary myotubes to demonstrate MET+LEU's skeletal muscle cell-autonomous properties.
Researchers have found that valosin-containing protein (VCP) is essential for KRAS-mutant pancreatic ductal adenocarcinoma cell growth and survival. Inhibiting VCP, combined with autophagy inhibition, enhances efficacy in preclinical studies.
A study in C. elegans suggests that disrupting meiosis in reproductive cells accelerates aging and triggers a decline in healthspan, similar to humans. The research highlights the importance of reproductive fitness for overall health, with potential applications for early detection and treatment of age-related diseases.
Scientists developed a new mouse line to study protein balance and quality control in the mammalian brain. The research revealed that different neurodegenerative diseases have distinct protein misfolding patterns, offering insights into potential therapeutic options.
Researchers at Northwestern University found that a damaged fertilized egg sends a molecular signal to the mother that protects her from cellular stress and environmental damage. This allows the mother to live longer and produce healthier eggs.
A signaling pathway that helps prevent protein aggregates in brain cells is also required for sleep in fruit flies and zebrafish, suggesting its presence in humans. The study found that suppressing this mechanism led to reduced sleep duration, while overproducing it caused increased sleepiness.
The University of Konstanz's Collaborative Research Centre 969 will continue its research in cellular proteostasis with a new funding period starting January 2020. The centre will focus on studying complex processes and networks of proteostasis, developing new techniques to make these processes visible and controllable.
A study published in eLife reveals that minocycline can increase the lifespan of aged roundworms by preventing the build-up of proteins, a mechanism that could be exploited to prevent neurodegenerative diseases. The antibiotic also reduces protein aggregation and extends lifespan in animals with impaired proteostasis.
Researchers will combine yeast, C. elegans models with mouse models to identify molecular changes in human aging and predict age-associated diseases such as Alzheimer's and Parkinson
Human embryonic stem cells are immortal due to a 'garbage disposal system' called the proteasome. Reducing E3-ubiquitin ligases levels does not affect their behavior, but impacts overall cell function.
Researchers found that the quality of protective molecular chaperones declines dramatically with age, accelerating decline in those with neurodegenerative diseases. A subnetwork of 28 critical genes provides a basis for biomarkers and new therapeutics to prevent protein damage and cell dysfunction.
Researchers at Scripps Research Institute have discovered a natural mechanism that cells use to protect mitochondria from damage, a key factor in neurodegenerative disorders and cancer. The study reveals that reducing the import of proteins into mitochondria can help protect these organelles during stress.
A NIH-funded study found that rapidly removing defective proteins can help protect brain cells from death. Researchers developed a new technique to track protein turnover in neurons, revealing differences in how individual cells handle proteins. This discovery may lead to improved treatments for neurodegenerative diseases.