Articles tagged with Dna Repair
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A diabetes drug has been found to improve DNA repair in cells affected by Xeroderma pigmentosum, a rare genetic disease. The drug, acetohexamide, degrades the DNA repair enzyme MUTYH, triggering an NER-independent mechanism for removing UV-induced DNA damage.
Researchers from the University of Seville studied a specific type of chromosomal break generated by enzymes called DNA topoisomerases. They found that this mechanism prevents the formation of aberrant chromosomal structures called translocations, which are linked to some types of cancer.
Researchers found that accurately transcribing DNA overrides DNA repair, with bacteria becoming hundreds of times more efficient at repairing DNA damage when the transcription fidelity factor GreA is absent. This discovery challenges traditional understanding and has significant implications for cancer research and evolution.
A team of scientists has identified a protein called TOX that drives the initiation and growth of an aggressive form of leukemia. TOX is expressed in 95 percent of human T-ALL cases and required for cancer's growth and persistence, offering new targeted treatment approaches.
Researchers have obtained the highest resolution map yet of human proteins critical to DNA function, providing insights into gene research and drug development. The study used cryo-electron microscopy to resolve the structure of transcription factor IIH at near-atomic resolution.
A new study reveals how the immune system avoids becoming cancerous by using a hair-trigger protein called Tia1. This protein controls the production of proteins needed to fix damaged DNA, allowing B cells to produce effective antibodies while preventing lasting harm.
A study by researchers at the Center for Genomic Regulation reveals that mistakes made by a DNA spellchecker can lead to cancer mutations. The findings suggest that high levels of alcohol and exposure to sunlight can shift the balance of DNA repair mechanisms, causing errors in critical parts of the genome.
A team of researchers has identified a new gene mutation associated with Fanconi anemia, a rare genetic disorder characterized by bone marrow failure. The mutation in RFWD3 gene was found to disrupt DNA repair mechanisms, increasing cancer risk in individuals with the disease.
Researchers have discovered how certain enzymes in living organisms can repair damaged DNA caused by prolonged exposure to UV light. The enzymes, called (6-4) DNA photolyase, use electrostatic interactions to bind to the damaged DNA and keep it separate from the rest of the cell.
Researchers at Osaka University have discovered a key role for protein SCAI in selecting between DNA repair mechanisms, NHEJ and HR, in response to damage. The study found that SCAI promotes the recruitment of HR proteins by binding to 53BP1.
A new gene mutation, RFWD3, has been linked to defective DNA repair and Fanconi anemia, a rare genetic disorder. The mutation was found in a 12-year-old patient without known Fanconi anemia genes, and cells from the patient showed increased susceptibility to DNA damage.
A new study reveals that tadpoles living in low-temperature environments are more susceptible to DNA damage from UV radiation. This increased risk can lead to mutations and cell death, contributing to the global amphibian extinction crisis.
Drexel University researchers uncover a crucial role of the Rad52 protein in RNA-dependent DNA repair. The study reveals an unexpected function of Rad52, promoting 'inverse strand exchange' between double-stranded DNA and RNA molecules. This mechanism may help identify new therapeutic targets for cancer treatment.
Ben-Gurion University researchers found that SIRT6 protein levels are significantly lower in Alzheimer's patients and contribute to the onset of the disease. The study suggests a link between low SIRT6 levels and DNA damage accumulation, which may lead to neurodegenerative diseases.
Researchers at IBS discovered a new function of DNA repair protein SHPRH, which regulates ribosome synthesis in response to nutrient availability. The protein's behavior changes during cellular starvation, allowing it to quickly recover ribosome production upon nutrient reintroduction.
Researchers at Aarhus University have described the structure and organization of the DNA control protein Rad26, revealing how kinase Rad3 is recruited to damaged DNA. This new knowledge may lead to the development of Rad3 inhibitors that make cancer cells more susceptible to chemotherapy.
A new study successfully uses CRISPR-Cas9 to modify the genome of Methanosarcina acetivorans, an archaeal species, for the first time. This breakthrough enables accelerated studies on these organisms, with implications for understanding global climate change and the global carbon cycle.
Scientists from UNC School of Medicine have confirmed the functions in bacterial cells of two important excision repair proteins, Mfd and UvrD, using an advanced sequencing technique. The study provides a genome-wide map of excision repair in bacteria and highlights the potential for developing novel antibiotic drugs.
Research reveals that stem cells from heavy smokers use error-prone DNA repair pathway, leading to accumulation of mutations and squamous cell carcinoma. The study suggests targeting DNA repair processes may be a promising approach to preventing and treating this form of lung cancer.
Researchers found that increasing niacin levels boosts NAD compound for energy generation and DNA repair, potentially protecting against Parkinson's. The study suggests repurposing cancer drugs to protect faulty mitochondria in Parkinson's disease.
Researchers have characterized the critical function of the Zf-GRF domain in manipulating DNA during repair processes. The domain is essential for APE2 enzyme activity, enabling it to bind to single-stranded DNA and facilitate its 3'-5' resection.
A recent study published in Genes & Development reveals an enzyme called UCHL3 that plays a crucial role in regulating the BRCA2 pathway. This research suggests that UCHL3 could be used as a potential therapeutic target to overcome chemotherapy resistance in breast and ovarian cancer cells.
A recent study found that hybrid structures composed of DNA and RNA play a crucial role in restoring genetic information after damage. The research also revealed that RNase H enzymes targeting these hybrids are vital for efficient DNA repair. This discovery offers potential for developing new cancer drugs targeting these enzymes.
A new study from the University of Pennsylvania has developed a system to observe the repair of broken DNA in telomeres, a process that drives 15% of cancers. The researchers found that this unique type of repair, called break-induced telomere synthesis, differs from other forms of homologous recombination.
Researchers at the University of Copenhagen have found that adding the substance NAD+ to mice and roundworms can extend life and delay aging processes. The study suggests that NAD+ plays a key role in maintaining cellular health and repairing genes, with potential benefits for patients with Alzheimer's and Parkinson's disease.
Researchers at the University of Pittsburgh School of Medicine identified a unique 'constrained motion' pattern in which Rad4, a repair protein, scans DNA for structural faults. This discovery could lead to therapies that enhance existing treatments and counter drug-resistance, particularly in cancer.
Researchers discovered that c-Jun N-terminal kinase (JNK) activates SIRT6 to repair broken DNA strands. The study found that JNK modifies a specific amino acid residue on SIRT6, allowing it to recruit the enzyme PARP1 to damaged sites.
Researchers found that mismatch repair machinery preferentially protects genetic integrity in open chromatin regions, increasing mutation rates in heterochromatic areas. This study provides direct evidence for the role of epigenetic systems in maintaining genetic fidelity.
Researchers at UC Berkeley discovered a way to boost CRISPR-Cas9 cutting efficiency up to fivefold by disrupting DNA repair mechanisms with short oligonucleotide pieces. This technique increases the success rate of creating knockouts, essential for studying gene function and correcting hereditary mutations.
A new technology called Maximum Depth Sequencing (MDS) can accurately read the order of DNA code and reveal how bacteria use high-speed evolution to defeat antibiotics. MDS also promises to enable earlier cancer diagnosis by detecting rare genetic changes in human cell populations.
Researchers have discovered a new molecular mechanism that directs cellular DNA repair proteins to lesions in DNA, making it an attractive target for cancer therapy. By understanding how this mechanism works, scientists can design small molecule inhibitors that block the function of TONSL protein and promote cancer cell death.
The IBS team identified baicalein as a suitable antagonist to battle malignant cancerous cells, binding to mismatched DNA and causing cancerous cells to self-destruct. The research found that baicalein significantly shrunk MutSα-deficient tumors in mice models, offering a viable option for patients with DNA MMR deficient tumors.
Sheffield scientists capture never-before-seen snapshots of enzymes trimming branched DNA after cell division. The discovery provides insight into the molecular process of DNA replication and repair, essential for all life forms.
The BRCA1 gene's ubiquitin ligase activity is crucial for error-free DNA repair through homologous recombination. Cells lacking this function are sensitive to DNA damaging agents and may develop cancer.
Researchers at Osaka University found that DNA damage response errors can lead to tumor formation when proteins are not removed correctly. Ku protein plays a key role in DNA repair, but its incorrect function can result in genetic information loss and cancer.
A study published in Science reveals that a molecule called ppGpp enables bacteria to repair damage to their DNA, including that caused by antibiotics. Adjusting the action of ppGpp may make bacteria more vulnerable to existing antibiotics, potentially yielding future solutions for antibiotic resistance and degenerative diseases.
Researchers created knockout mice that lack a gene involved in DNA repair, shedding light on how cells fix broken DNA. The mice developed kidney and liver dysfunction due to impaired detoxification, highlighting the importance of FAN1 protein.
Researchers have made significant discoveries about the RTR complex's role in DNA repair and its connection to cancer development. The study highlights the importance of maintaining genomic stability during reproduction.
Researchers have identified a molecular target for DNA repair defects behind Fanconi anemia, a complex genetic disorder responsible for birth anomalies, organ damage, anemia, and cancer. The study reveals a potential therapeutic strategy and raises important questions about a compensatory DNA repair process.
Researchers found that BRCA1 depletion impairs brain cell function and contributes to cognitive decline in Alzheimer's disease. The study suggests that therapeutic manipulation of BRCA1 may prevent neuronal damage and cognitive decline in patients with Alzheimer's disease or at risk for the disease.
Research suggests that low levels of BRCA1 protein in the brain may contribute to dementia. The study found that adding amyloid beta to neurons lowers levels of BRCA1, increasing DNA damage and cognitive decline. Further research is needed to determine whether BRCA1 may be a potential therapeutic target for treating dementia.
Researchers have identified a previously unknown protein that plays a vital role in DNA repair, potentially leading to new biomarkers and treatments for cancer. The discovery could help prevent errors during the repair process, reducing the risk of mutations and cancer.
A study led by Indiana University biologist Patricia Foster found that external environmental forces and oxidation are the primary threats to DNA repair, unlike previously thought. The research used whole genome analysis of spontaneous mutation in E. coli and showed that only loss of oxidative damage repair significantly impacted mutat...
Researchers at Rockefeller University have made new discoveries about the DNA repair process, uncovering previously unknown functions of histone H2AX. They found that a specific portion of the protein interacts with phosphorylated H2AX, facilitating the repair of double-stranded breaks in DNA.
Researchers from LMU Munich have discovered that human DNA repair enzymes employ a 'pincer' strategy to target damaged DNA, using a sugar molecule as a key component. This finding sheds new light on the complex process of DNA repair and its importance in maintaining genome stability.
A new study by Joslin researchers reveals that alterations in the DNA damage checkpoint pathway machinery and higher levels of miR200 are associated with severe complications in type 1 diabetes. This finding holds promise for early detection and treatment of complications through therapeutic interventions targeting miR200.
Scientists at MD Anderson Cancer Center discovered the critical role of fumarase enzyme in DNA repair, revealing a key mechanism for reversing genetic damage leading to cancer and therapy resistance. The study's findings have potential implications for developing new cancer treatments by inhibiting DNA-PKs and fumarase.
Researchers at Lomonosov Moscow State University discovered a new DNA repair mechanism that can detect and fix single-stranded breaks in histone-bound DNA. This breakthrough opens up new avenues for treating neurodegenerative diseases such as Alzheimer's.
Researchers at Max Planck Institute of Biochemistry have analyzed the protein composition of the DNA replication machinery in response to damaged DNA. They found that over 90 proteins are recruited to aid in repair, including many known factors as well as new proteins with unknown functions.
Researchers discovered that damaged DNA with expanded CAG repeats relocate to the periphery of the cell nucleus for repair. This shift is crucial in preventing repeat instability and genetic disease.
Researchers at UNC School of Medicine have created a method to find where DNA repair happens throughout the entire human genome. This breakthrough could lead to better and more effective cancer drugs or improvements in existing ones.
Researchers identified a protein called ATM that regulates DNA repair during sperm production, preventing genetic errors that can cause infertility. The discovery sheds light on the mechanisms controlling gamete formation and has implications for understanding human fertility.
Two proteins critical for maintaining healthy day-night cycles also protect against mutations that could lead to cancer. The study found that these proteins have an unexpected role in DNA repair, stabilizing a protein called Cry1 and preventing errors in DNA transcription.
Scientists at MD Anderson Cancer Center have discovered a key DNA pathway that allows certain brain cancers to resist standard treatments. The study found that activation of this pathway leads to enhanced survival of tumor cells and increased DNA repair, contributing to treatment resistance.
A study found Sall4 protein promotes DNA repair in embryonic stem cells, potentially aiding cancer cell survival. This discovery raises the possibility of targeting Sall4 for cancer treatment.
A study analyzing 17 million mutations in 650 cancer patients found that genetic mistakes are better repaired in some parts of the human genome, with genes switched on having lower mutation rates. The 'mismatch repair' mechanism varies in efficiency depending on chromosome regions.
Researchers discovered that organs have varying DNA repair capabilities, with the heart exhibiting the highest capacity, followed by other tissues. The brain showed no ability to repair damaged DNA, leading scientists to suggest that this may be linked to memory loss and dementia.
Researchers at the University of Illinois at Chicago found that damaged DNA can cause a molecule to slow down its patrol, giving it more time to recognize and initiate repair. The protein XPC, important for DNA repair, stalls at damaged sites due to twisted damage, allowing it to open and fix the damage.
Researchers at Imperial College London have taken pictures of the BRCA2 protein, showing how it repairs damaged DNA and interacts with other proteins. The study reveals that BRCA2 works in pairs with RAD51 to assemble filaments on broken DNA strands.
Researchers found that an ancient protein-making enzyme, TyrRS, has a second major function: protecting DNA during cellular stress. This discovery could lead to better therapies for radiation injuries and hereditary disorders like Charcot-Marie-Tooth disease.