Articles tagged with Dna Repair
Researchers found radiotherapy induces consistent genomic damage through DNA deletions, which can lead to poor outcomes. Targeting error-prone DNA repair mechanisms may enhance radiotherapy efficacy.
Researchers discovered that acute myeloid leukemia cancer cells depend on the Fanconi anemia pathway, which can be inhibited to kill cancer cells. This finding could lead to more effective and safer cancer treatments.
Researchers identify a new class of mibefradil-based DNA repair inhibitors, which could be further advanced into pre-clinical testing and eventually clinical trials for glioblastoma radiosensitization. The compounds retain potency as DNA repair inhibitors while demonstrating reduced hERG and CYP450 enzyme inhibition.
A University of Seville group discovered the mechanism by which BRG1 inactivation leads to genetic instability and tumour formation. The study reveals that the SWI/SNF complex plays a crucial role in resolving chromosomal conflicts, and its mutation can cause DNA replication defects and chromosomal breaks.
An international study reveals that the MutS protein, known as the guardian of our genome, coordinates the essential DNA repair process from beginning to end. The researchers used cryo-electron microscopy to visualize the protein and describe its mechanism of action.
A new study by Salk scientists identifies specific regions of the genome that neurons prioritize for DNA repair, revealing
Three UNIST graduate students, SangIn Kim, ByeongEun Lee, and YeonSong Choi, have been awarded the prestigious 2021 Asan Foundation Medical Bioscience Scholarship for their innovative work in DNA damage response, degenerative brain diseases, and disease genomics. The award provides financial assistance and recognizes their contribution...
Scientists discovered the structural and molecular factors governing the stability of a protein complex involved in DNA repair pathways. The study reveals that exposure to organic solvents and oxidizing environments can cause the complex to disassemble, offering insights into novel phenomena and potential treatments for diseases such a...
A team of researchers at Tokyo Institute of Technology has identified a critical protein segment responsible for activating the MRN complex, a key player in DNA repair. The discovery reveals a conserved function across species, with implications for genetic disorders and gene editing applications.
Researchers describe for the first time the full sequence of Biologist-induced replication (BIR) and found it stalls at roadblocks when transcription is introduced near the beginning. This discovery suggests that BIR's high risk-reward arrangement may contribute to genomic instability leading to cancer development.
A study published in Molecular Cell found that blocking ALC1 enzyme can selectively kill cancer cells with homologous recombination deficiency, offering a potential new treatment option for certain types of breast and ovarian cancers. The researchers also identified ALC1 as a key factor in determining patient survival rates.
Scientists studying DNA damage repair process aim to identify a protein that can help healthy cells avoid dying or becoming cancerous. ATF3, a sensor of cell stress, has been shown to be essential to efficient DNA repair and may be the key to developing new cancer therapies.
Researchers discovered a new protein called cryptochrome that repairs DNA damage caused by ultraviolet radiation, a function previously attributed to photolysis in cells. This breakthrough highlights how proteins can evolve and acquire new functions over time.
Researchers have identified the structure of double-strand DNA break repair by PARP enzymes, which can bridge broken DNA ends together. The study provides insight into the mechanisms underlying PARP activation and catalytic cycle, potentially aiding in understanding resistance to cancer drugs that inhibit PARP.
A team of scientists has discovered how the enzyme SPRTN recognizes and cleaves DNA-protein crosslinks, which are formed when proteins attach to DNA. This new mechanism is crucial for cell viability and the suppression of tumorigenesis, and has implications for cancer therapy.
Researchers created a novel bioluminescent system to monitor DNA double-strand break (DSB) repair pathways, which play a crucial role in multiple conditions including cancer. The BLRR-based system allows for direct tracking of DSB repair pathways in animals and cell lines, providing new insights into cancer treatment resistance.
Research from NC State University reveals how MutL and MutS proteins create an immobile structure to prevent replication errors, reducing errors by a thousand-fold. The complex also prevents mismatched regions from being packed back into the cell during division.
Scientists at Johns Hopkins Medicine have developed a light-activated CRISPR system that allows for targeted DNA cutting within seconds. The new technology reveals new details about the DNA repair process, which may aid in understanding aging and cancer.
Researchers screened 163,000 DNA mutations in C. elegans roundworms to understand the interplay between DNA damage and faulty repair systems. The study found that multiple DNA repair pathways work together to prevent mutagenesis, and a single mutagen can leave varying mutational signatures depending on the faulty repair system.
Researchers analyzed over 2700 C. elegans genomes to understand the causes of mutations. They found that DNA damage and inaccurate repair mechanisms can lead to mutations, which are a root cause of cancer. The study challenges the assumption of a single cause for mutational signatures in cancer genomes.
Researchers discovered that helper proteins Swi5-Sfr1 and Rad51-related helpers collaborate to activate Rad51 in DNA repair. Mutations in Swi5-Sfr1 compromised activation, but yeast cells lacking Rad51-related helpers still repaired DNA, suggesting a compensatory role.
Australian scientists have identified a motor protein called CHD4 that helps cells access DNA information when needed. The discovery provides insights into how defects in this process contribute to diseases such as schizophrenia and cancer.
Researchers discovered a crucial DNA repair process in yeast that involves a protein called Rad51 and two helper proteins called Swi5-Sfr1. This finding may help understand why DNA repair processes fail to function properly in humans, leading to diseases like cancer and inherited conditions.
Researchers have discovered a novel 'toolkit' of proteins that can repair breaks in DNA, which can lead to cellular ageing, cancer, and neurological diseases. The discovery of the protein TEX264 holds promise for treating cancer and preventing age-related diseases.
Researchers at the University of Toronto have found a complex system of filaments and liquid droplet dynamics that enables the repair of damaged DNA in cell nuclei. This discovery challenges previous assumptions about DNA damage and highlights the value of cross-disciplinary research.
A new study finds that low doses of DEHP impair egg production in roundworms by increasing DNA double-strand breaks and hampering repair systems. This can lead to chromosomal defects and embryonic development problems.
A new study reveals a new tool that can analyze CRISPR edits in just 48 hours, identifying multiple outcomes of the process. The tool detects subtle mutations to DNA near the site of repair, which may have no consequence for patients but are essential to gauge patient risks.
A team of scientists has identified the tools for repairing damaged DNA molecules, revealing new insights into how the human genome works. The study found that damaged DNA undergoes a unique packing state during repair, moving faster than healthy DNA but depending on its size.
Researchers from the La Jolla Institute for Immunology identified a new role for HMCES in alternative end-joining, a secondary strategy used by mammalian cells to rejoin severe cuts across both strands of DNA. This discovery suggests that HMCES is versatile enough to accomplish entirely different tasks in response to DNA damage.
Scientists from the University of Copenhagen have identified two proteins, 53BP1 and RIF1, that orchestrate the repair of damaged DNA by building a three-dimensional scaffold around broken strands. This scaffold concentrates special repair proteins, enabling cells to prevent collateral damage and maintain genetic stability.
Researchers at Moffitt Cancer Center have identified a new mechanism controlling DNA repair, where βarrestin-1 targets 53BP1 for protein degradation. This finding provides a novel strategy for developing therapeutic agents with radiation protection properties.
DNA molecules have a hydrophobic interior that groups together when exposed to water, controlling the binding process. The discovery opens doors for new understanding in medicine and life sciences, with potential applications in fighting resistant bacteria and curing cancer.
Patrick Sung, a leading BRCA expert, has received the National Cancer Institute's Outstanding Investigator Award, providing $6.1 million through 2026. His work focuses on understanding BRCA biology and its role in cancer initiation and progression.
Scientists discovered that club lung cells can repair damaged DNA and survive influenza infection, but this resilience may also contribute to chronic obstructive pulmonary disease and asthma. The findings suggest a double-edged sword in the battle between cells and viruses.
Researchers have made a groundbreaking discovery about the alpha-synuclein protein's function in repairing DNA breaks, which may lead to new treatments for Parkinson's disease and other neurodegenerative disorders. The study reveals that alpha-synuclein plays a critical role in binding broken strands of DNA within the cell's nucleus.
A protein called UV-DDB has been found to identify and supervise the repair of DNA damage, suggesting a key role in maintaining genome stability. The discovery sheds light on why some individuals with a rare genetic disorder are more susceptible to cancer.
DNA damaged by cisplatin is mostly fixed within two circadian cycles in noncancerous tissue, with repair of transcribed genes dominating the first 48 hours. This knowledge could aid the design of successful chronochemotherapies to reduce toxicity and target cancer cells.
Researchers from the Thomä group at FMI have identified a new mechanism by which UV-DDB detects and binds to damaged DNA tightly packed in nucleosomes. This mechanism, known as 'slide-assisted site-exposure', allows repair proteins to bind to lesions without requiring additional proteins or chemical energy.
A Yale study reveals how cediranib, a cancer drug of limited use, stops certain cancer cells from repairing their DNA to survive. The combination of cediranib with olaparib may deliver a lethal blow in cancers that rely on a specific DNA repair pathway.
The study discovered that the 'longevity gene' SIRT6 is responsible for more efficient DNA repair in species with longer lifespans. This gene's enhanced activity in organisms like beavers contributes to their extended lifespan, highlighting a potential target for anti-aging interventions.
A team of scientists at the Gladstone Institutes has developed a reliable method to identify potential off-target effects in therapeutically relevant cell types. The DISCOVER-Seq technique uses DNA repair factors to pinpoint exact sites where CRISPR cuts occur, enabling more accurate genome editing.
Researchers developed a molecular bait to identify proteins involved in the cell's choice of DNA repair pathway, revealing key enzymes for homologous recombination. The discovery opens new possibilities for targeted cancer treatments using PARP inhibitors.
Researchers created a lab-grown population of E. coli bacteria that became resistant to ionizing radiation through genetic mutations and enhanced DNA repair mechanisms. This breakthrough could lead to the development of radiation-resistant bacteria for environmental clean-up, cancer therapy protection, and astronaut protection in space.
A study published in Cell Reports reveals the role of protein PIF1 in repairing G-quadruplex DNA structures, which can impede DNA repair mechanisms. The discovery sheds light on potential therapeutic options for cancer treatment and could improve patient outcomes.
A new Collaborative Research Center will explore cellular mechanisms involved in protecting and repairing genes. The study aims to determine factors causing genomic instability, signaling pathways detecting DNA damage, and mechanisms of protection against DNA damage.
Researchers found a species of blind cavefish lacking an ancient DNA repair system, previously known only in placental mammals. The discovery supports the 'nocturnal bottleneck' theory, suggesting ancestors of modern mammals lived in darkness before dinosaurs.
A breakthrough discovery reveals that the DDX11 helicase enzyme plays a vital role in DNA repair and serves as a backup to the Fanconi Anemia pathway. This finding has significant implications for understanding genomic stability and disorders associated with DNA repair deficiency, including cancer and developmental disorders.
Researchers found that the CSB protein, previously thought to be solely responsible for DNA repair, also enhances acetylation of alpha-Tubulin and regulates autophagy. HDAC inhibition restores balance, improving skin symptoms in mouse models. Further studies aim to explore its potential treatment for Cockayne syndrome.
Researchers found that RUNX proteins bind to DNA damage sites and co-regulate the recruitment of DNA repair protein FANCD2. This discovery could lead to the development of synthetic-lethal approaches to attack RUNX-deficient cancers, including solid tumours of the breast and leukemia.
Researchers discovered that the Fanconi anemia DNA repair pathway plays a crucial role in fixing CRISPR breaks and increasing the efficiency of homology-directed repair. This new understanding could help boost CRISPR-Cas9 editing's success rates, particularly for treating diseases like sickle cell anemia.
A team of researchers has uncovered a new protein complex called Shieldin that plays a critical role in normal cell division and cancer treatment. The complex shields broken DNA ends and controls the type of DNA repair system used by cells, making it vulnerable to targeting by PARP inhibitors and platinum-based chemotherapies.
A new study reveals that a DNA repair protein associated with cancer can disrupt electron transport through DNA, leading to mutations. The researchers found that a specific mutation in the MUTYH protein causes the iron-sulfur cluster to degrade when exposed to oxygen.
Scientists at the University of Sheffield have discovered an enzyme called UCHL3 that regulates DNA repair and may hold promise in improving treatment for chemotherapy-resistant cancers. The findings also suggest a link between UCHL3 activity and brain ageing, which could impact memory, cognitive function, and learning.
A recent study published in Nature Communications reveals that the enzyme USP48 plays a crucial role in DNA repair and may hold promise as a therapeutic target for Fanconi Anemia. Inactivation of USP48 in FA-deficient cells restores nearly error-free repair of damaged DNA.
Researchers measured DNA repair in mice treated with cisplatin over a 24-hour period, finding nearly 2,000 genes repaired according to the circadian clock. This study suggests that understanding the interaction between circadian clocks and DNA repair could lead to more effective chemotherapy regimens.
Researchers developed MAGESTIC to refine gene-editing process, enhancing precision and increasing cell survival rates by sevenfold. The new platform enables precise editing of genetic variants, helping uncover impact on cellular function and disease susceptibility.
A new study casts doubt on a leading theory for bdelloid rotifers' evolution, suggesting DNA repair following desiccation may not be key to their success. The researchers found no evidence of the predicted differences between species that can and cannot survive desiccation.
Researchers discovered that plant DNA repair works more efficiently on active genes, which are transcribed into RNA and proteins. The system's efficiency varies according to the day/night cycle, reflecting normal daily variations in transcription activity.
A University of Córdoba research group has disproved a widespread assumption among geneticists regarding DNA structure. The study reveals that two types of gaps caused by spontaneous and deliberate breakage are not equivalent, contradicting previous understanding.
Researchers have solved a longstanding puzzle of how cells compact DNA to enable healthy cell division. They found that single cells can compact DNA 10,000-fold by forming series of compacted loops and anchoring them to a central spiral axis.