Articles tagged with Dna Damage Responses
A Goethe University-led study reveals how mutations in the SPRTN enzyme cause chronic inflammation and premature ageing. The research team found that damaged DNA in the cell nucleus leaks into the cytoplasm, activating defense mechanisms and leading to chronic inflammation.
Researchers found that mutations in the CFAP410 gene change its interaction with another protein, making motor neuron cells more vulnerable to DNA damage and cell death. This discovery provides new insights into the mechanisms underlying Motor Neurone Disease and highlights potential targets for new therapies.
Researchers found that Fen1 protein improves cell tolerance to alovudine by counteracting the toxic effect of 53BP1. This discovery promises new cancer treatments and biomarkers for cancerous cells with Fen1 deficiency.
Researchers developed a chemical probe that binds to damaged mitochondrial DNA, blocking enzymatic processes that lead to its degradation. This approach lessens mtDNA loss, preserving energy production in vulnerable tissues. The new molecule successfully reduced inflammation and maintained functional DNA despite chemical tagging.
Scientists at San Raffaele Telethon Institute for Gene Therapy discovered that CRISPR-Cas9 gene editing can cause inflammation and senescence-like responses in blood stem cells. This reduces the cells' ability to regenerate blood cells after transplantation, limiting the long-term success of gene therapy.
Researchers have discovered that inhibiting the metalloprotease ADAM19 can reduce gut inflammation and cell aging markers across species. The study found that blocking ADAM19 reduced gut damage and inflammation in fruit flies, mice, and human cells, offering a promising path for creating treatments to maintain healthy tissues.
A research team has uncovered a reciprocal regulatory relationship between extrachromosomal DNA maintenance and the DNA damage response in tumor cells. The study found that ecDNA actively replicates and is stably maintained in ecDNA-positive cells, triggering the ATM-mediated DDR pathway.
The treatment demonstrated early signals of efficacy, with 65.7% of patients experiencing lasting stable disease, and was generally well-tolerated, with most adverse events being mild and manageable.
Neuro-immunologist Stephen Hauser has won the 2025 Breakthrough Prize in Life Sciences for his role in identifying the immune system's primary driver of damage to nerve cells in multiple sclerosis. His B-cell theory has led to the development of therapies that have transformed treatment, reducing relapses and improving prognosis.
PARP inhibitors have been found to be effective in treating cancers with BRCA1/2 mutations by blocking DNA repair pathways. The combination of PARPis with chemotherapeutic drugs can also improve treatment efficacy, increasing DNA damage and blocking repair processes.
Researchers have developed a new strategy to protect cancer patients from radiation-induced DNA damage using a protein from tardigrades. The approach makes use of messenger RNA encoding the protein, which is delivered to patient tissues before radiation treatment. This reduces double-stranded DNA breaks by 50% in mouse models.
Researchers found that a rare genetic syndrome causes different damage mechanisms in male and female brains, affecting neurogenesis and energy production. The study suggests that the ADNP protein plays a crucial role in brain development and aging, with distinct functions in males and females.
Researchers reveal senescence's impact on liver health, from repair and regeneration to chronic disease progression. Emerging therapies, such as senolytic treatments, aim to selectively eliminate senescent cells while preserving healthy tissue.
Researchers found RNA damage triggers inflammation and cell death in skin after UV exposure. The ribotoxic stress response, orchestrated by protein ZAK-alpha, plays a key role in this process.
Researchers discovered that DNA repair determines how cancer cells die following radiotherapy, with specific pathways triggering cell death noticed by the immune system. Blocking these pathways can force cancer cells to die in a manner that alerts the immune system, leading to new potential treatments.
UC Irvine researchers have identified a previously unknown mechanism that triggers an inflammatory immune response in cells with damaged DNA. This discovery may lead to more effective cancer treatments by allowing doctors to personalize therapies tailored to individual patients' needs.
A comprehensive study examining over 16,000 necropsy records from 292 vertebrate species found significant differences in cancer prevalence. Cancer rates increase with body size and cellular mutation rates but decrease with longer gestation periods.
Researchers at Colorado State University have identified an alternate method to study changes during the DNA replication process in lab settings using genetically modified yeast. This new approach provides a less toxic and quickly reversible alternative to hydroxyurea, allowing for better insight into cell cycle arrest mechanisms.
A new study found that common breast cancer treatments, including chemotherapy, radiation, and surgery, can increase expression of aging markers in breast cancer survivors. The study suggests that these treatments can have a more extensive impact on the body than previously thought, leading to accelerated biological aging.
A new mechanism of DNA damage response has been identified, involving an RNA transcript that regulates genome stability. The study found that NEAT1, a long non-coding RNA transcript, plays a crucial role in recognizing and repairing DNA double-strand breaks.
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 new study found that 2-bromopalmitate treatment reverses cell senescence in human vascular smooth muscle cells, reducing DNA damage markers and promoting cell proliferation. The research suggests a critical role for protein palmitoylation in regulating the senescent phenotype.
Researchers have made significant progress in understanding the function of APE1 in DNA damage response, showing that it promotes SSB-induced ATM DDR through two mechanisms. The study provides direct evidence for APE1's active role in activating ATM kinase to promote the repair of single-strand DNA damage.
A recent study by Johns Hopkins Medicine reveals that the ZAK protein is a critical player in the cell's response to UV radiation damage, determining whether cells live or die. The research, published in Cell, suggests that companies developing drugs targeting ribosomes may find ZAK to be a driver of cell death across cancer types.
Researchers at Howard University have identified a new therapeutic strategy to combat prostate cancer by depleting amino acids. This depletion induces oxidative stress and DNA damage in cancer cells, making them more susceptible to treatment with DNA repair-targeted and immune checkpoint blockade therapies.
When E. coli detects damage from antibiotic Ciprofloxacin, it sends out an SOS signal that alters cellular activity. The bacteria then mutate their DNA to repair the damage or adapt to resist the antibiotic. Researchers studied this process in detail using bioreactors and found all genes are activated simultaneously at the protein level.
A new study reveals sex-specific effects of germline regulation on longevity and somatic repair in vertebrates. Removing the germline extends male lifespan and improves stress resistance in females.
Scientists have discovered that aging clocks measure stochastic changes in cells, rather than damage accumulation. This finding suggests that aging can be predicted using the variation in cellular processes.
Researchers found that SARS-CoV-2 spike protein interrupts p53-MDM2 interaction but does not bind with p53 protein in cancer cells. The study also shows that SARS-CoV-2 spike suppresses p53-dependent gene activation, leading to increased cell viability after chemotherapy exposure.
Researchers at the University of Toronto have discovered a DNA repair mechanism that uses nuclear metamorphosis to fix double-strand breaks in human cells. This discovery has significant implications for cancer treatment and premature aging, and may lead to new therapeutic avenues.
Researchers at UNC-Chapel Hill have found that tardigrades can increase DNA repair genes' production in response to radiation, making them more resilient to damage. This discovery could lead to new ideas on protecting other animals and microorganisms from damaging radiation.
Researchers at Nagoya University discover aldehydes cause DNA damage and contribute to premature aging in humans. The team proposes a link between aldehyde-derived DNA damage and premature aging, highlighting potential targets for therapeutic intervention.
Four studies conclude that longer genes are most susceptible to aging due to increased potential sites for DNA damage. Long genes have more sites for damage, making them prone to degradation with age, contributing to conditions like Alzheimer's disease.
Researchers have discovered that PR55α, a regulatory subunit of PP2A phosphatase, inhibits p16 expression and blocks cellular senescence induction by γ-irradiation. This finding provides a new insight into the regulation of the p16/RB pathway in response to stressors.
A team of researchers found that diffuse anaplasia (DA) subtype of Wilms tumor grows despite high DNA damage and TP53 mutation, leading to resistance to chemotherapy. The study suggests that DA histology emerges through accumulating DNA damage and CNAs, creating selection pressure for TP53 mutations.
Researchers identified gartisertib as a potent ATR inhibitor that enhances cell death in patient-derived glioblastoma cell lines. The study also showed synergy between gartisertib and TMZ+RT treatment, with higher sensitivity to gartisertib observed in MGMT promoter unmethylated cells.
A team of scientists has identified a previously unrecognized control point in DNA repair processes, which could lead to novel cancer therapies by inhibiting the repair of damaged cancer cells. The newly discovered GSE1-CoREST complex contains three enzymes that control DNA repair and may form the basis for improved cancer treatments.
Researchers have found that a specific pathway, cGAS-STING, is unleashed to prevent cancer formation by detecting DNA damage within cells. The discovery reveals the 'key' to unleashing this pathway, which can potentially reactivate it to treat and prevent breast cancer development.
Researchers have identified a gene that links deafness to cell death in the inner ear, creating new opportunities for preventing hearing loss. The discovery suggests that UPR-blocking drugs could prevent deafness caused by loud noise exposure or aging.
This study found that SIRT6 activation improves DNA damage repair efficiency and reduces baseline DNA damage in chondrocytes from older donors. MDL-800 treatment also lowered p16 promoter activity and decreased DNA damage in murine cartilage explants, supporting the concept of SIRT6 as a critical regulator of DNA repair.
Researchers at Salk Institute uncover a mechanism for repairing damaged nerves during peripheral neuropathy, with protein Mitf playing a key role. The findings have the potential to inspire novel therapeutics that bolster repair function and heal peripheral neuropathy.
Researchers have identified a new mechanism for removing RNA-protein crosslinks induced by aldehydes, which can damage cellular function. This discovery sheds light on the effects of aldehydes on human cells and may be particularly important for maintaining cell function in older individuals.
Researchers identified key factors in DNA repair, revealing the 'proofreading' portion of polymerase epsilon helps prevent strand breakage. This knowledge arms scientists with ways to enhance anti-cancer drug effectiveness and develop new diagnostic methods.
Researchers developed a human in vitro model of radiation-induced lung injury, closely mimicking the complexities of the disease. The Human Lung Alveolus Chip recapitulates hallmarks of RILI, including DNA damage, inflammation, and injury to lung cells and blood vessels.
A new specimen collection system has been developed to enhance assisted reproductive technologies by providing a simple one-step method for selecting high-quality sperm for ICSI. The system, known as NovaSort, uses a barrier mesh to isolate mobile sperm without damaging their DNA.
Researchers combined three highly potent cancer drugs in a single prodrug that is activated in tumor cells, resulting in improved efficacy and reduced side effects. The new approach has shown promise as a potential solution to reduce the burden on patients' bodies during cancer treatment.
Researchers developed a DNA damage-induced senescence model in osteoarthritic chondrocytes, which reliably induces cellular senescence and accumulates senescent cells in OA joint tissues. The study provides a useful model to develop therapeutic approaches targeting senescence in osteoarthritis.
A newly discovered fungus has been found to transform the toxic compound patulin into less harmful byproducts, offering potential solutions for controlling its presence in food products. The fungus, identified as Acremonium sp., was shown to degrade patulin into desoxypatulinic acid and other compounds, which are significantly less toxic.
The oldest and fastest evolving moss in the world, Takakia, may not survive climate change. Despite its rapid adaptation capabilities, the species is declining in population size due to warming temperatures and increasing UV radiation, threatening its very existence.
Research by Professor Björn Schumacher investigates the role of male germ cells in genetic mutations. The study suggests that paternal DNA damage can lead to faulty repairs in the genome, resulting in structural variants.
The nucleus is metabolically active and uses antioxidant enzymes to repair DNA damage. Cells relocate mitochondrial machinery to the nucleus in response to DNA damage, highlighting a paradigm shift in cellular biology.
A study by Tufts University researchers reveals how DNA repair can fail near expanded repeats, leading to mutations and disease. The team found that certain proteins play a crucial role in stabilizing the DNA during repair.
Researchers at Tokyo Medical and Dental University identify a novel focal adhesion remodeling process that strengthens cell-matrix adhesion in response to genotoxic stress. This mechanism involves the replacement of FAK with FRNK, leading to increased firm cell attachment.
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.
Scientists from the University of North Carolina at Charlotte review nucleolar DNA damage response pathways to combat cancer. By attacking these mechanisms, researchers aim to disrupt cancer's reproduction and growth.
Researchers at Ulsan National Institute of Science and Technology (UNIST) have observed quasiparticles in a classical system made of microparticles driven by viscous flow. The hydrodynamic forces among the particles create pair excitations that propagate through the crystal, stimulating the creation of new pairs.
A new study by researchers at Florida Atlantic University explored the effects of resistance training on older adults' cellular level. The study found that resistance training did not significantly affect inflammatory proteins or redox balance markers, but showed a significant reduction in a specific protein ratio. This may support the...
A Phase Ib clinical trial found that sequential administration of PARP inhibitor olaparib and WEE1 inhibitor adavosertib is safe and well-tolerated, with promising signs of anti-tumor activity in patients with advanced cancers driven by DNA damage response mutations. The combination showed durable responses in patients with resistant c...
Researchers have discovered that neurons with double-stranded breaks (DSBs) in their DNA actively trigger an inflammatory response, which is mediated by the activation of the NFkappaB transcription factor. This process elicits an immune response from microglia, leading to synaptic loss and cognitive function impairment.
Researchers at Nagoya University have identified new agents involved in DNA damage tolerance pathways, including RFWD3, which may contribute to anticancer treatment. The study's findings suggest that inhibiting these pathways could sensitize cancer cells to conventional chemotherapeutic agents.