Articles tagged with Double Strand Breaks
Flinders University researchers discovered a biological process that could explain some stillbirths and pave the way for early detection. The study found that molecules called circular RNAs build up in the placenta too quickly during pregnancy, compromising its ability to nourish the baby.
A small protein involved in neurodegeneration leading to Parkinson's disease also drives a type of skin cancer known as melanoma, according to new research. The study suggests new avenues for drug development to reduce the risk of developing both diseases by targeting alpha-synuclein.
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.
Scientists have cracked the code of meiotic DNA double-strand breaks, a crucial process for genetic diversity and chromosomal segregation. The study reveals that Mg2+ is essential for DNA cleavage activity and functions independently of ATP.
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 Osaka University have developed a new gene editing technique called NICER, which significantly reduces off-target mutations compared to traditional CRISPR/Cas9 methods. This novel approach uses multiple small cuts in DNA strands and promotes interhomolog homologous recombination to correct heterozygous mutations.
Researchers discovered that MSH2-MSH3 plays a crucial role in selecting the right DNA repair process by interacting with other proteins during DSB repair. This interaction facilitates error-free homologous recombination and blocks error-prone polymerase theta-mediated end-joining.
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.
Researchers at Rice University and St. Jude Children’s Research Hospital discovered the structural basis of DNA polymerase theta-mediated microhomology-mediated end joining, a process complementary to homologous recombination and non-homologous end joining. This mechanism could be a promising target for precision cancer therapy.
Researchers found that reducing SAMHD1 levels made brain tumor cells sensitive to chemotherapy drugs and slowed cell growth. They also suspect that glioblastoma alters SAMHD1's function to aid its own survival and treatment resistance.
Researchers at Kyoto University have discovered a phosphorylation pathway that regulates meiotic double-strand break activity, ensuring genome stability. Enzymes ATR kinase and PP4 phosphatase work together to maintain a balance of DNA breaks, allowing for successful meiosis.
Experimental study finds large DNA insertions caused by retrotransposition can increase cancer risk in human cells edited with CRISPR/Cas9. In contrast, base editing and prime editing show much lower rates of retrotransposition.
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.
Scientists have developed a new therapy called CINDELA, which employs CRISPR-Cas9 to kill cancer cells while leaving normal tissues intact. The treatment targets specific mutations found in cancer cells and induces cell death through DNA double-strand breaks.
A new method identifies proteins binding to R-loops, revealing the role of DDX41 in regulating R-loop levels and preventing DNA damage. Elevated R-loop levels increase cancer risk.
Researchers at Princeton University developed a novel method called Repair-seq to understand genome editing tools, revealing complex mechanisms of DNA repair. This work improves the CRISPR gene-editing method by identifying new pathways and optimizing systems.
Researchers from Osaka University found that protein phosphatase 1 binds to RIF1 at broken DNA ends, blocking proteins that create single-stranded DNA tails, and promoting the non-homologous end joining repair pathway. This novel mechanism helps protect double-strand breaks from developing a tail, which is what Shieldin binds to.
A new study found that memory formation causes neurons to break their DNA, leading to changes in gene expression and potentially undermining brain health with age. The study also discovered that glia play a significant role in establishing memories from fear conditioning.
Cells introduce hundreds of DNA DSBs to facilitate genetic recombination, but researchers found that approximately 20% of breaks correspond to closely positioned pairs of DSBs, which can initiate recombination at chromosome gaps
Researchers at Northwestern University used cryo-electron microscopy to visualize DNA breakage sensing and repair, gaining new insight into the process. The study's findings could potentially form the basis for understanding how cells respond to chemotherapy and radiation, leading to improved cancer treatments.
The Ballistic Simulated Bifurcation Algorithm (bSB) and the Discrete Simulated Bifurcation Algorithm (dSB) can solve large-scale combinatorial optimization problems up to 20,000 times faster than current machines, achieving near-optimal solutions in record time.
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.
Researchers have discovered that DNA resection pathways are highly specific and designed to repair distinct types of DNA damage, challenging the notion of redundancy in these mechanisms. This understanding has significant implications for cancer therapy and the development of new treatments.
Researchers at Memorial Sloan Kettering Cancer Center have figured out how X and Y chromosomes pair up properly during meiosis. They discovered that a repeated sequence of DNA in the pseudoautosomal region (PAR) attracts double-strand break-related proteins, leading to frequent DNA breaks in this region.
Researchers have elucidated the complete three-dimensional structure of the MR complex, a molecular machine responsible for detecting and repairing DNA damage. The new structure reveals how the complex binds to DNA and initiates repair processes, shedding light on the intricate mechanisms involved.
Researchers found that low-dose X-ray treatment does not induce genome instability or DNA damage in stem cells. Instead, these cells proliferate and maintain their health, contradicting previous assumptions about the harm caused by ionizing radiation.
Researchers at Salk Institute create a new version of CRISPR/Cas9 that can activate genes without creating DNA breaks, potentially treating diseases such as diabetes and muscular dystrophy. The technology operates epigenetically, influencing gene activity without changing the DNA sequence.
Researchers discovered that prolonged exposure to ionizing radiation can delay cell cycle and increase DNA repair efficiency, with potential implications for cancer risk reduction. The study found that human stem cells can activate alternative DNA repair mechanisms, such as homologous recombination, in response to prolonged irradiation.
A new study found that DNA breakage is a natural process that allows the brain to learn and generate memories, but weakens with age. Researchers discovered that DNA damage can lead to increased expression of genes involved in learning and memory, which could be detrimental as we age.
Researchers discovered that double-strand breaks occur at replication fork stalling sites due to collision. The study found that non-homologous end-joining is the primary repair method used in this context, despite its potential for errors.
A new platform called GUIDE-seq detects unwanted DNA breaks induced by CRISPR-Cas RGNs across the entire human genome. The method is sensitive enough to detect off-target sites at a frequency as low as 0.1 percent in a population of cells.
Researchers at Gladstone Institutes found that a certain type of DNA damage can occur during normal brain functions such as learning. The team identified two therapeutic strategies that reduce disruptions to this process, which is associated with Alzheimer's disease.
Researchers at Berkeley Lab found evidence of non-linear DNA damage response to low dose radiation, suggesting a non-proportional relationship between dose and cancer risk. The study used time-lapse live imaging to observe the formation of DNA repair centers, which may be an optimal way for cells to deal with sparse damage.
Researchers at Kyoto University have designed an inexpensive new material capable of quick and accurate detection of carbon dioxide gas. The compound gives off variable degrees of visible light in correspondence with different gas concentrations, enabling the development of easy-to-use monitoring devices.
Scripps researchers have discovered the Nbs1 component of the Mre11-Rad50-Nbs1 complex, which helps cells repair severe DNA damage. The complex is critical in preventing cancer development and can also repair diseased cells targeted by chemotherapy.
The study discovered a mechanism that switches on genetic instability in cancer cells, leading to growth advantage and invasion. The researchers developed an assay to determine the efficiency of DNA repair mechanisms, which could lead to developing ways to switch off this mechanism.
The structure of the Mre11 protein bound to DNA has been revealed, showing how it recognizes and remodels broken DNA strands. This breakthrough provides insight into the essential function of Mre11 in homologous recombination, a critical method for repairing double-strand breaks.
Researchers have found that double-strand DNA breaks occur more frequently in specific regions near telomeres and centromeres, increasing the likelihood of chromosome gene swapping. This discovery may lead to a better understanding of developmental chromosome abnormalities and birth defects.
Studies show that double-strand breaks and radiation-induced foci occur at specific regions of the nucleus for repair, contradicting previous assumptions of random distribution. The findings suggest a time effect, with microscope images showing nonrandom distribution of RIF within five minutes of exposure to high-energy particles.
Researchers identified a short tandem array of telomeric repeats bound by a Rap1/Trf2 complex as sufficient to impede non-homologous end joining at human telomeric DNA ends. This finding opens the door to understanding mechanisms that initiate genomic instability in cancer cells.
St. Jude researchers used a new technique to monitor the movement of DNA repair proteins as they interacted with each other and gathered at the site of damage. The study found that disruption of these proteins can cause mutations, cell death, or cancer, providing critical insights into DNA repair mechanisms.
Researchers identified a unique stretch of internal telomeric repeats that suppress the DNA damage checkpoint response. The arrest duration was significantly shorter than expected, indicating a potential mechanism for preventing normal telomeres from being recognized as damaged DNA.