Articles tagged with Dna Replication
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Researchers found that DNA polymerases derived from E. coli are more prone to errors under microgravity, increasing the mutation rate and potentially leading to cancer. The study's results highlight the importance of designing rotating spaceships with artificial gravity to prevent negative effects on astronauts' health.
Cryo-EM study reveals details of DNA repair mechanism translesion synthesis (TLS), allowing cells to survive with mutations. Key protein complex Pol K - PCNA interaction modulated by ubiquitination facilitates recruitment of TLS polymerase to damage sites.
Scientists successfully induce gene expression from a synthetic DNA and evolution through continuous replication using cell-free materials. They also improve the DNA to increase its replication efficiency by up to 10-fold in just 60 days.
Researchers discovered a DNA modification system that coordinates bacterial replication in TB. The DarT/DarG system can be targeted by new antibiotics, offering hope for treating the deadly disease.
Yang Gao's lab has received a $1.9 million NIH grant to investigate the mechanisms of proteins that produce copies of genomic DNA, with potential implications for cancer treatment. The research aims to understand how DNA replication and repair processes can be targeted to develop new therapies.
Researchers have developed a new method to measure DNA torsional stiffness, which can impact how cells work. The technique provides insights into the biological implications of twist-induced phase transitions in DNA.
The study shows that the CTD and OD domains of mtp53 R273H play key roles in mutant p53 GOF, pertaining to processes associated with DNA replication. The authors investigated the role of these domains in cell proliferation, DNA replication, and cell cycle progression in breast cancer cells.
A study by Nagoya University researchers reveals that cohesin's ring needs to open for certain processes, like DNA replication and chromosome segregation. This opening facilitates the progressive replication of the DNA double helix and allows DNA looping, crucial for regulating gene expression.
A new study reveals that cyanobacteria rely on a circadian clock to precisely time DNA replication. Disruptions to this rhythm can lead to unfinished chromosomes and potential health problems. The findings have implications for understanding the impact of interrupted circadian rhythms on human health.
A recent study published in Molecular Biology and Evolution reveals that the DNA replication machinery of Mimivirus, a giant virus, is ancient and evolved over time. The research suggests that Mimiviral genes related to DNA replication are subject to purifying selection, indicating their essential role in the organism's survival.
Researchers have identified a critical role for DNA replication timing in controlling the packing of DNA with its regulatory factors, known as the epigenome. The study found that disrupting this program can lead to inappropriate cellular functions and negative health outcomes.
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.
Researchers at Cold Spring Harbor Laboratory have discovered how human cells assemble and disassemble Origin Recognition Complexes to initiate DNA replication. The study reveals a specific interaction between ORC1 protein and CDC6, allowing them to work together in a coordinated manner.
Researchers have discovered a 19-amino acid insertion helix in the Orc4 subunit of yeast ORC that enables human-like DNA binding, transforming yeast into a humanized ORC. This finding provides new insights for cancer therapy and human development, including potential targets for anti-cancer drug screening.
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.
Researchers at Arizona State University have discovered that certain molecules can promote the self-assembly of sliding clamps into structures containing many stacked doughnut shapes, resembling tubes of doughnuts. These findings suggest a new mechanism by which cells may control DNA replication under stress conditions.
Researchers from the University of Copenhagen have discovered how MCM proteins regulate DNA replication pace and preserve essential skill for life continuation in cells. Their findings suggest a potential way to exploit cancer weaknesses by manipulating molecular roadblocks that slow down DNA replication.
Researchers used a genome database to identify the cell type from which cancers derive, revealing new insights into cancer development. By comparing cancer cells to normal human cells, they found that different cancers mostly closely matched specific cell types, shedding light on their origins and tumor behavior.
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.
Researchers found that a gene's checkpoint mechanism can sometimes allow cells to divide abnormally, leading to worse damage. This discovery has important implications for treating cancer and understanding the inner workings of cells.
Researchers visualize DNA replication in single human cells, revealing a non-random selection mechanism for replication activation on CTCF-organized chromatin structures. The study provides critical insights into the role of local epigenetic environment in coordinating genome duplication.
Researchers at NUI Galway have discovered a key role for CDC7 in cancer cell replication, providing new insights into developing novel treatments. The study found that blocking CDC7 could be an effective strategy for treating aggressive cancers like pancreatic and colon cancer.
An international team studied the Pol δ-DNA-PCNA complex to understand DNA replication and how it can malfunction. The team found that PCNA acts as a platform for different processing enzymes, similar to a toolbelt with an array of tools.
DNA repair mechanisms choose between pathways to limit harmful chromosomal combinations that may be predisposed to cancer and genetic diseases. The study found Rad52-dependent single-strand annealing leads to gross chromosomal rearrangements at centromeres, while Rad51 promotes conservative non-crossover recombination.
Cancer cells rely on different factors for survival when DNA replication is blocked. Researchers found that inhibiting a key protein called Cdc7 selectively kills cancer cells by inactivating their safety mechanism. This discovery provides a new strategy for targeting cancer cells and developing anti-cancer agents.
Scientists have identified a molecular mechanism that could reverse the genetic defect responsible for Friedreich's ataxia by enhancing a natural process that contracts repetitive DNA sequences in living tissue. This contraction occurs during DNA replication and is triggered by the formation of an unusual triple-helical DNA structure.
The study found that H2A.Z promotes H4K20me2 deposition, recruiting ORC1 to license and activate early DNA replication origins. H2A.Z-regulated origins have higher firing efficiency and earlier replication timing compared to other origins.
ATAD5 plays a crucial role in counteracting DNA replication stress by regulating PCNA unloading and promoting RAD51 recruitment. This study reveals ATAD5's fundamental mechanism of replication stress control, contributing to the development of cancer therapy.
Two research teams deciphered how RNase H2 and RNase H1 are coordinated to remove RNA-DNA hybrid structures from chromosomes. The study found that RNase H2 primarily acts during the G2 phase after DNA replication, while RNase H1 can act in all phases of the cell cycle.
Researchers created a mutated form of DNA repair protein RAD51 to study its critical functions at stalled replication forks. The study found that RAD51's strand exchange activity is not required for fork regression, but is crucial for restarting replication once the obstacle has been removed.
Researchers found that intrinsic mechanical properties of chromatin determine how fibers entwine during DNA replication, preventing tangles and ensuring proper segregation. The study highlights the importance of physical principles in biological processes and provides new insights into chromatin behavior.
Researchers at LMU Munich propose a direct mechanism for synthesizing DNA subunits from organic compounds in a prebiotic environment. This process could have given rise to DNA strands on early Earth, potentially 4 billion years ago.
A novel molecular mechanism for regulating PCNA cycling during DNA replication has been discovered. The ATAD5-RFC-Like-Complex (ATAD5-RLC) is a PCNA unloader that opens the PCNA ring to remove it from DNA.
Researchers have established a novel method to study DNA replication in individual cells, allowing them to gain insights into the mechanisms that maintain genomic DNA stability. The 'scRepli-seq' method revealed that genome replication profiles were highly conserved among cells and reflected the organization of chromatin compartments.
A new study led by Grant Brown suggests that at times of stress, DNA replication errors are far more frequent than previously appreciated. This could lead to increased mutations in human cells, potentially contributing to cancer and other diseases.
Scientists have discovered two methods to mend DNA-protein crosslinks and established how DNA replication triggers these repair processes. The researchers hope their findings can be used to develop more efficient combination treatments for cancer cells.
Researchers have identified specific points along the DNA molecule that control replication, shedding light on a decades-old mystery. This discovery could lead to breakthroughs in understanding genetic diseases where replication timing is disrupted.
Researchers found that vorinostat effectively inhibited HPV DNA amplification and virus production in preclinical experiments. Additionally, the treatment induced programmed cell death in infected cells. The study suggests that HDAC inhibitors could be promising compounds for treating benign HPV infections.
Researchers have discovered how DNA gyrase, a molecular machine in bacterial cells, prevents twists in DNA that can stop replication and kill the cell. This knowledge can lead to the design of new targeted antibiotics to combat antibiotic-resistant bacteria.
Researchers discovered that loss of tumor protein p53 promotes cancer development by allowing cells to replicate despite growth stimuli deficiencies. This discovery provides insight into how cancer cells survive and multiply in adverse conditions.
The study reveals that the WD40 repeats in AND-1 prevent nascent DNA cleavage by a nuclease, allowing for successful cell division. The discovery highlights the crucial function of AND-1 in protecting replicated DNA from degradation during replication and cell proliferation.
Researchers found liver cells do not need ORC1 to replicate DNA, a key component of cell division. This process, called an endocycle, allows cells to copy their DNA multiple times without dividing, resulting in larger cells with more DNA. Understanding this mechanism could help explain how cancer arises and how it spreads.
The team found that telomeres are regulated by proteins, including Taz1, which tether internal regions to the telomeres. This process ensures faithful duplication of genetic material. Better understanding of this mechanism may inform research into maintaining genetic information and preventing diseases.
Researchers identify TLK1 and TLK2 as critical for accurate DNA replication, preventing extensive damage and cell death. The study found that these enzymes are rarely mutated in cancers but their high expression correlates with poor patient outcomes.
Researchers at Indiana University have identified 'hotspots' in DNA where genetic mutations are significantly elevated, including areas with repeated chemical letters and specific patterns of three letters. This study provides a roadmap for identifying similar trouble spots in human DNA.
Researchers have determined the atomic structure of the Origin Recognition Complex (ORC) bound to DNA, revealing its role in selecting replication origins. The study reveals that ORC selects DNA sites based on their unique structure rather than specific base sequences.
Researchers at Saint Louis University have uncovered new answers about why cells rapidly age in children with a rare disease called Hutchinson-Gilford Progeria Syndrome. The team found that cellular replication stress and a mistaken innate immune response are culprits, and successfully blocked these processes with vitamin D.
A recent study by George Mason University researchers found that women who have given birth have shorter telomeres compared to childless women. The study suggests a link between having children and increased telomere shortening, which may be associated with higher morbidity and mortality rates.
Mutated Cyclin E and Myc genes induce premature DNA replication, leading to molecular collisions and new mutations. The study identified a method to map replication origins on all chromosomes, revealing that aberrant sites can cause genomic instability in cancers.
Researchers have discovered a molecular commonality between two progeroid syndromes and introduced a method for disease recognition that could lead to breakthroughs in therapy. By characterizing disruptions in DNA replication timing, the team identified a shared abnormality in the gene TP63.
Scientists mapped the flow and regulation of nucleotides, revealing a mechanism that slows down DNA replication when out of rhythm. This slowdown allows for nucleotide production to catch up, ensuring healthy genome copying without mistakes.
Scientists at Van Andel Research Institute and collaborators have shed new light on the critical step of DNA replication, revealing a spring-loaded mechanism that positions DNA strands toward two side-way gates. This discovery offers fresh insights into a fundamental process of life and driver of many different diseases, including cancer.
Researchers at Scripps Research Institute have developed a method for creating modified DNA-based hydrogels with unique properties. These hydrogels can be dissolved, reformed, and retain their biochemical activity, making them suitable for various applications such as drug delivery and cell growth.
Scientists from TU Delft and colleagues show that condensin, a protein involved in packing DNA into chromosomes, has motor function. This discovery supports the 'loop-extrusion' model of chromosome packing, suggesting that condensin pulls DNA inwards to create loops.
Researchers found that impaired DNA replication can lead to genome-wide epigenetic changes, resulting in the inheritance of new gene expression states for up to five generations. These epigenetic alterations establish new gene expression patterns that can be passed down through multiple generations.
Researchers developed a new imaging approach called ChromEMT to visualize the three-dimensional structure of chromatin, resolving long-standing debates about its organization. The study reveals that local nucleosome structure combined with global 3D organization determines gene expression and cell fate.
Researchers watched individual DNA strands replicate and found that polymerases on the leading and lagging strands are completely autonomous, with no coordination. The study reveals a new stochastic view of DNA replication, challenging conventional wisdom and providing insights into this essential biological process.
Researchers discovered Rrm3 protein's role in repairing breaks during DNA replication, a process crucial for preventing genetic instability and cancer. This finding sheds light on the physiological mechanisms that prevent genetic instability.
Researchers discovered Corynebacterium glutamicum can implement multifork mode of DNA replication, enhancing its growth rate. The discovery also revealed the bacterium's diploid condition confers advantages in repairing DNA damage and stress responses.
Researchers have discovered that excessive DNA replication can lead to cell malignancy but also offers a potential approach against cancer. By exploiting the cooperation of proteins CDC6 and CDT1, scientists aim to induce lethal DNA re-replication selectively in cancer cells.