Articles tagged with Dna Repair
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.
Researchers investigated the central role of Sae2 in regulating yeast DNA repair. A recent study found that Sae2 controls Mre11 endo- and exonuclease activities via different mechanisms, essential for maintaining genetic information.
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.
Professor Helle Ulrich will investigate how a small regulatory protein called ubiquitin contributes to DNA replication and repair, and decipher how cells direct different pathways. The ERC Advanced Grant aims to gain a deeper mechanistic understanding of ubiquitin's function in preventing mutations that can cause ageing and cancer.
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.
Researchers at PNRI reveal how specific DNA rearrangements called inverted triplications contribute to the development of various genetic diseases. These complex rearrangements are caused by segments of DNA switching templates during the repair process, leading to disruptions in normal gene function and contributing to genetic disorders.
A new study found that combining histone deacetylase inhibitors, poly (ADP ribose) polymerase inhibitors, and decitabine resulted in synergistic cytotoxicity in all cell lines tested. This combination impaired DNA repair pathways and altered epigenetic regulation of gene expression.
A team of researchers from Xi'an Jiaotong-Liverpool University has engineered a short sequence of artificial DNA to target the mutant protein p53-R175H, linked to lung, colorectal, and breast cancers. The new molecule, dp53m, inhibits cancer cell growth and increases sensitivity to chemotherapy agent cisplatin.
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 have uncovered important details about the role of CSB/ERCC6 and CSA/ERCC8 genes in Cockayne syndrome. These genes encode enzymes associated with DNA repair that initiate transcription-coupled repair of toxic DNA-protein crosslinks, marking and breaking down damaged DNA.
Researchers have deciphered trabectedin's precise mechanism of action, revealing its ability to induce persistent DNA breaks in cancer cells. This disruption of the transcription-coupled nucleotide excision repair (TC-NER) pathway leads to long-lasting DNA breaks that ultimately kill cancer cells.
A protein called PARP1 forms a special healing zone that holds loose DNA ends together and allows DNA repair to begin. This discovery provides valuable insight into the molecular basis of DNA damage repair and its potential application in cancer treatment.
Researchers have discovered that RecA protein repairs breaks in double-stranded DNA without unwinding the helix, leading to a new understanding of homologous recombination. This breakthrough has significant implications for breast cancer research and may lead to new treatments.
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.
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 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.
Mayo Clinic researchers found that cells expressing PD-1 and PD-L1 within a certain distance of each other can predict the success of immunotherapy in patients with colorectal cancer. This spatial analysis may help select patients most likely to benefit from treatment, improving outcomes and minimizing unnecessary treatments.
A Duke University team has found that retrotransposons use the cell's DNA repair function to create a ring-like shape and then produce a matching double strand. This discovery challenges long-held theories about retrotransposons being byproducts of bad gene copying.
Researchers have discovered that gene editing technologies may introduce unintended mutations and damage to DNA in early human embryos. The study found that most cells repair breaks in the DNA using non-homologous end joining, which can lead to additional genetic abnormalities.
A new study reveals that the protein complex BCDX2 plays a critical role in DNA repair, suggesting mutations in this complex could lead to cancer. The research also highlights the importance of screening for mutations in people with a family history of breast and ovarian cancers.
Researchers at UC San Diego have discovered that shattered DNA fragments are tethered together during cell division, allowing them to be reassembled in a different order. Destroying the tether may help prevent cancerous mutations and is now being explored as a therapeutic target.
A new study reveals the molecular mechanism behind bacterial DNA repair, showing that RNA polymerase plays a key role in identifying and fixing errors. Researchers found that RNaseHII cooperates with RNA polymerase to scan for misincorporated ribonucleotides in living bacterial cells.
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.
A University of Colorado at Boulder research team has discovered a protein crucial for repairing DNA in cancer cells, which they found can be selectively targeted to kill cancer cells without harming healthy ones.
A new study reveals the mechanism of BRCA2's DNA repair function, understanding its role in breast and ovarian cancer development. The findings also provide insights into developing targeted cancer therapies by inhibiting DNA repair mechanisms.
Researchers at University of Cologne discovered a way to improve DNA repair in body cells, making them resilient towards DNA damage. This can help prevent aging and cancer development, with potential applications for treating human patients.
Scientists discovered a new type of DNA repair mechanism that cancer cells use to recover from next-generation cancer radiation therapy. DNA polymerase θ (POLQ) is an important factor in repairing complex DNA double-strand breaks, and inhibiting POLQ may augment the efficacy of heavy ion radiation therapy.
Researchers at Pusan National University have developed a novel FRET-based biosensor to detect double-strand breaks in DNA, providing real-time information on γH2AX. The sensor's sensitivity is higher than conventional immunostaining techniques, making it useful for identifying DNA damage factors and elucidating repair mechanisms.
A team of researchers has discovered a potential therapeutic that can synergize with existing drugs to more effectively kill certain leukemia cells. The therapy targets a DNA repair protein and shows promise in clinical trials.
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 team of researchers from Michigan State University has discovered two distinct DNA-PK protein complexes that have different roles in DNA repair. One complex fills in lost information, while the other activates enzymes to remove damaged ends. This finding may lead to new strategies for therapeutic gene editing and cancer diagnostics. ...
Researchers used C-trap technology to investigate how different DNA repair proteins identify and bind to their respective forms of damage. They found that some proteins arrived at the damage site together and departed together, while others showed surprising variability in their association and dissociation patterns. The study provides...
A team at Harvard Medical School identified a novel mechanism of DNA repair that occurs exclusively in neurons, allowing them to maintain their function over time despite intense repetitive work. The NPAS4–NuA4 complex initiates a pathway to repair DNA breaks induced by neuronal activity.
Researchers found a molecular staple called NIHCOLE that helps liver cancer cells repair broken DNA, making them resistant to radiotherapy. Understanding this mechanism may lead to the development of new strategies to combat liver cancers with poor prognosis.
Researchers at KAUST have discovered the molecular mechanisms of DNA repair by studying the interaction between two enzymes, Lig1 and PCNA. Lig1 seals nicks in DNA by attaching to a ring-shaped protein called PCNA, which dislodges another enzyme FEN1 to prepare for sealing.
Researchers found that SIRT6 maintains mitochondrial function through transcription regulation of mitochondrial genes. Without SIRT6, mitochondrial gene expression is down-regulated, leading to increased ROS production and impaired ATP generation, similar to changes observed in aging and neurodegenerative diseases.
A recent study has unveiled how nucleotide excision repair (NER) is controlled at the molecular level, shedding light on its role in cancer treatment. The research revealed that TFIIH uses XPG to stimulate motor activity and locate damaged DNA, licensing XPG nuclease activity to excise it.
The German Research Foundation renewed CRC 1361 for an additional four years to explore mechanisms of DNA repair and genome stability. The consortium aims to elucidate how cells safeguard genetic information and promote human health by understanding DNA damage signaling pathways.
Researchers identify POLQ's vital role in responding to DNA replication stress and its potential as a cancer target. Inhibiting POLQ may limit mutation diversity and cancer evolution, offering new hope for cancer treatment.
Researchers at Kyoto University discovered METTL16's role in DNA repair and erythropoiesis, a process generating 200 billion new red blood cells daily. Tiny methyl groups on specific mRNAs play a pivotal role in this process, involving mechanisms mediated by RNA-binding proteins.
In a recent study, researchers targeted the POL theta enzyme to inhibit DNA production in cancer cells. The approach represents a new method for developing specific therapies for patients with BRCA1 mutations.
A new study by Weill Cornell Medicine investigators discovered that error-prone DNA replication and repair may lead to mutations and cancer in individuals with BRCA1 gene mutations. The team identified a faulty DNA repair mechanism called microhomology-mediated break-induced replication (MMBIR) as a key contributor to genomic instabili...
A team of researchers found that chromatin motion on damaged DNA sites moves faster than those away from damage, with the group moving as a unit over short distances. This coherent movement is crucial for effective DNA repair, preventing damaged DNA from harmful contact and improving accuracy.
EdU, a common DNA labeling molecule, triggers a runaway DNA repair process that is fatal to cancer cells, including those in the brain. This discovery opens up new possibilities for using EdU as an anticancer agent, particularly for fast-dividing cancerous brain cells.
A recent study published in Cancer Research identified a unique vulnerability in certain high-risk cancers that can be exploited for targeted therapy. Researchers found that cancer cells with alternative lengthening of telomeres (ALT) have a common weakness, leading to resistance to DNA-damaging agents and chemotherapy.
A mutated zebrafish eye provides a glimpse into the role of banp in preventing cell death and regulating the cell cycle. The study found that banp promotes the expression of 31 genes involved in DNA repair, tumor suppression, and cell duplication.
The research team will analyze the remaining two enzymes necessary for riboflavin production and build a 'riboflavinator' in a test tube. This understanding could lead to improved methods for treating diseases and improving public health.
A new CRISPR strategy, employing natural DNA repair machinery, provides a foundation for novel gene therapy strategies to cure genetic diseases. The technique, known as homologous chromosome-templated repair, uses "nicks" of single DNA strands to correct genetic defects.
A recent study published in Aging-US reveals the crucial role of WRN in making choices between classical and alternative non-homologous end joining (NHEJ) DNA repair pathways. The research provides new insights into progeroid syndromes, such as Werner syndrome, and their connection to aging.
Biologists at the University of Rochester have identified two key systems controlling gene expression related to longevity: circadian networks regulating negative lifespan genes and the pluripotency network controlling positive lifespan genes. This research provides new insights into understanding how longevity evolves and may lead to ...
Researchers have developed biodegradable nanovesicles that efficiently encapsulate and deliver PARP1 siRNA to breast cancer tumors in mice, inhibiting oncogene expression and extending survival. The polymersomes, assembled from three biodegradable block copolymers, have strong potential for precision-targeted therapeutic carriers.
Researchers at the University of Birmingham have discovered two new DNA repair genes, SETD1A and BOD1L, which can make cancer cells more sensitive to radiotherapy. These findings may lead to improved treatment efficiency and patient outcomes by allowing clinicians to identify targeted treatments for specific patients.
Researchers at Medical University of South Carolina found that blocking the enzyme polymerase reduces the virus's ability to multiply. This discovery exposes an Achilles' heel that could be targeted with a therapeutic. Polymerase is a key tool for DNA replication and repair, making the virus vulnerable to disruption.
Researchers found that a critical enzyme called AAG plays a crucial role in making cells respond to stress by communicating between different parts of the cell. This new understanding could lead to improved cancer treatments using alkylating agents, a class of drugs commonly used in chemotherapy.
A new study from MIT suggests that genome loops, which were believed to play a crucial role in controlling gene expression, are actually short-lived and fleeting. The researchers found that these loops only exist for about 3-6% of the time and last for only 10-30 minutes.
Scientists have redefined how bacterial cells repair damaged DNA, finding that RNA polymerase plays a central role in the process. The discovery challenges existing theories and has implications for medicine, as many antibiotics and chemotherapies work by damaging DNA.
Scientists at Van Andel Institute and Rockefeller University have revealed the structure of the 911 DNA checkpoint clamp, which loads onto DNA to repair damage. The novel finding shows that the 911 clamp is loaded onto DNA from the opposite end, a surprise in the field of DNA replication.
University of Ottawa scientists, collaborating with Yale researchers, have discovered the hidden influence of a single variation between histone H3.1 and H3.3 proteins. This finding could expand our understanding of DNA damage repair and its role in diseases like cancers and sponastrine dysplasia.
Two clinical trials will report groundbreaking data on adjuvant olaparib for germline BRCA1/2 associated breast cancer and pembrolizumab for early-stage non-small cell lung cancer. These treatments aim to improve survival rates and reduce recurrence.
Researchers have discovered a mechanism to increase the effectiveness of base excision repair (BER), a pathway involved in repairing damaged DNA. By capturing polymerase beta at a precise point in the cell life cycle, the enzyme creates new genetic material 17 times faster, suggesting an interlocked function between its two roles.