Articles tagged with Homologous Recombination
Philip Tai, PhD, received a $1.6 million grant to investigate AAV vector mechanisms using high-resolution DNA sequencing technology. His findings could lead to new vector designs that improve gene therapy treatments' safety. The goal is to remove mutations that cause cancer-causing integration into host cells.
Researchers found that DNA loops facilitate homologous recombination, a key DNA repair process linked to cancer. These loops enable the repair machinery to scan for an intact copy of the damaged region more efficiently.
Researchers have developed 'molecular scissors' that can precisely and permanently disable the hepatitis B virus's hidden genetic material. The treatment has shown promising results in laboratory tests and HBV-infected mice, with a 99% reduction in circulating viral DNA. This innovation represents a significant step towards a functiona...
Researchers have revealed the structural mechanisms of a major DNA repair pathway in human cells, showing how RAD51 filament promotes strand exchange and facilitates DNA repair. The study provides fundamental insights into biochemical reactions of eukaryotic homologous recombination.
A Phase II trial found durable antitumor activity in patients with BRCA1/2 mutations treated with olaparib and pembrolizumab, with 8.3% complete response rate
Researchers have discovered a new mechanism of how anticancer drugs attack and destroy BRCA mutant cancer cells, including drug-resistant breast cancer cells. The study found that small DNA nicks can expand into large single-stranded DNA gaps, leading to cell death.
Research reveals that bacteria form species through a process called homologous recombination, which exchanges genetic material across the entire genome. This exchange acts as a cohesive force, keeping members of the same species similar and maintaining distinct species boundaries.
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.
A new study by UT Health San Antonio reveals that BRCA1 plays a crucial role in promoting error-free DNA repair through the activation of end resection enzymes. This understanding sheds light on the tumor suppressor function of BRCA1 and has important implications for breast and other cancers.
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.
Researchers unveiled a previously unknown effect of PG545 in ovarian cancer cells, inducing DNA damage and promoting autophagic degradation of RAD51. This breakthrough could aid in selecting the most appropriate treatments for ovarian cancer patients with PARPi resistance.
Researchers have developed a novel tool for the selective and efficient recovery of large DNA molecules using TAR cloning. This technique has been applied to isolate individual gene alleles, study genome architecture and evolution, and engineer synthetic viruses with novel properties, including vaccine development.
A research team sheds light on Dmc1 filament assembly mechanisms using single-molecule experiments. Swi5-Sfr1 and Hop2-Mnd1 proteins regulate Dmc1 assembly through distinct mechanisms, promoting efficient strand exchange during homologous recombination.
Researchers have identified LP-284 as a novel acylfulvene compound with anti-tumor activity against non-Hodgkin's lymphoma. The compound exerts nanomolar potency in 15 NHL cell lines and prolongs survival of mantle cell lymphoma xenograft mice, making it a potential therapeutic option for patients with HR or TC-NER deficiency.
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.
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.
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.
A new study explores the characteristics of 36 basic variants of the Holliday junction, a fundamental building block used in DNA nanoforms. The results show that sequences forming the four protruding arms of the junction can enhance or hinder crystallization processes.
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.
Researchers used mutant mice to study meiosis, which forms eggs and sperm, revealing that breaks in DNA can lead to unanticipated types of harmful mutations. The study found that when there are too many double-strand breaks, they may not be repaired properly, leading to potentially severe mutations.
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.
Berkeley Lab researchers find XPG plays a critical role in maintaining genome stability, raising the possibility that it prevents breast and ovarian cancers. The protein interacts with BRCA1 and BRCA2 to carry out homologous recombination repair.
Researchers found that cancer cells lacking BRCA1 compensate by reducing 53BP1 levels, which allows them to resume homologous recombination and grow. The study suggests a new pathway for how breast cancer cells lose 53BP1, enabling resistance to chemotherapy and potentially identifying patients who respond to cathepsin inhibitors.
Researchers at Berkeley Lab have discovered a new process for repairing double-strand breaks in heterochromatin, a crucial step in maintaining genome stability. This mechanism allows cells to accurately repair DNA damage and prevent chromosomal abnormalities that can lead to cancer and birth defects.
Researchers at Iowa State University have developed a new technique for making genetic changes in plant genes, allowing for targeted manipulations with high efficiency. This process harnesses homologous recombination to precisely introduce DNA at predetermined locations, enabling faster and safer gene editing for various crops.
Researchers have found that RAG-1 mediated cleavage occurs on one allele at a time during V(D)J recombination, ensuring allelic exclusion. This process is crucial in preventing translocations, a common underlying mechanism for leukemias and lymphomas.
Two protocols, one for DNA repair homologous recombination and another for sumoylation of proteins, are featured in CSH Protocols. These methods provide a biochemical means to dissect the mechanisms of molecular processes involved in DNA repair and post-translational modification.