Articles tagged with Dna Replication
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A recent study by Caltech and Vanderbilt University researchers found that electrons play a crucial role in DNA replication, allowing the cell to quickly locate and repair mutations. The discovery reveals a new pathway for cells to regulate DNA replication, which is essential for maintaining genome stability.
Researchers have mapped the critical steps of DNA replication, revealing how a ring-shaped protein called origin recognition complex (ORC) initiates the process by slipping into a groove on DNA and initiating a cascade of microscopic interactions. The study provides new insights into an immensely complex system that is constantly ongoi...
Researchers found that hairpin structures can effectively replicate DNA, leading to faster evolution. This discovery challenges traditional views of DNA replication and provides insight into the origins of life on Earth.
A new study identifies a gene, DONSON, responsible for microcephalic dwarfism by revealing its crucial role in DNA replication. Cells with faulty DONSON genes struggle to replicate DNA correctly, leading to growth defects typical of the disorder.
A new study reveals the structure of DNA helicase at the replication fork, reversing a long-held assumption about its orientation. The findings provide a crucial piece in understanding how life propagates and may lead to new treatments for diseases such as cancers and anemias.
Researchers have solved the mystery of DNA replication by identifying a ring of proteins that binds to origin DNA, causing it to melt and initiate replication. This discovery could lead to understanding genetic duplication and potentially blocking viral pathogens and cancer cells.
Researchers discovered a possible explanation for the occurrence of large-scale DNA expansions that cause over a dozen neuromuscular and neurodegenerative disorders. These expansions are controlled by genes involved in repairing DNA breaks, leading to the formation of extra repeats.
Researchers from Lomonosov Moscow State University have discovered the mechanisms of DNA packaging in the cell nucleus, which has implications for epigenetic control of gene expression. The study reveals that chromatin structures maintain high levels of packing and flexibility despite traditional notions.
A research team has solved the three-dimensional structure of PrimPol, a key protein that helps damaged cellular DNA repair itself. The knowledge gained from this study will likely aid in designing anti-cancer agents.
Researchers have developed a novel method to rapidly screen hundreds of chemicals for their anti-cancer properties by harnessing the power of knotted DNA structures. By detecting the activity of an enzyme crucial to cancer cell survival, this technique offers a promising tool for identifying potential new treatments.
A recent study from Cold Spring Harbor Laboratory sheds light on the critical decision every newly born cell makes: whether to continue proliferating or exit the cell-division cycle. The decision depends on delaying the expression of Cyclin E, which is regulated by a feedback loop involving ORC1 and CDC6.
Researchers found that head-on collisions between DNA replication and transcription increase mutation rates, particularly in the promoter region. This susceptibility can lead to genetic changes affecting an organism's health, from bacteria to humans.
Cells use programmed fork arrest to halt DNA replication at terminator sites, controlling life span and preserving genome stability. The process involves proteins working together to calibrate fork movement, preventing constant machinery operation.
Researchers at Newcastle University have identified a new essential sequence within bacterial genomes required for DNA replication, dubbed the DnaA-trio. This discovery sheds light on a fundamental biological process shared among all living organisms and opens doors to studying enigmatic replication origin elements in higher organisms.
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.
A study by University of Minnesota researchers reveals a pathway that enables cancer cells to tolerate faulty DNA replication, potentially leading to new anti-cancer therapies. The discovery was made possible by the development of a tool to analyze protein regulation triggered by DNA errors.
Researchers proposed a new mechanism for DNA replication called the 'pumpjack' mechanism, which involves a molecular machine with two distinct conformations that rock back and forth to split the DNA double helix. This linear translocation mechanism appears different from previously thought mechanisms in more primitive organisms.
Research at Indiana University identifies a genetic mechanism that drives cancer-causing mutations by mutating genes during DNA replication. APOBEC3G, an enzyme known to trigger harmful changes, may cause these mutations by targeting cytosines in single-stranded DNA on the lagging strand template.
A team of Swiss and Russian scientists has deciphered how APOBEC takes advantage of a weakness in DNA replication to induce mutations, primarily affecting early-replicating genes. The study reveals that APOBEC targets single-stranded DNA regions during replication, which are more prone to mutations.
In a breakthrough study, researchers discovered how search-and-rescue proteins like MutS identify and correct rare DNA mutations that can cause certain cancers. The findings provide insight into the mechanism of DNA mismatch repair and could lead to new methods for detecting and preventing cancer.
The project aims to analyze core replication complexes crucial for repairing damaged DNA and understanding cancer initiation and progression. The study may lead to insights into human health and disease, particularly cancer susceptibility.
Researchers from North Carolina State University have discovered how two important proofreader proteins, MutS and MutL, work together to signal the body's repair mechanism. The proteins use a unique communication system involving PCNA, which helps them identify and correct errors during DNA replication.
Scientists from HKUST and Tsinghua University solved the structure of the MCM2-7 Complex using Cryo Electron Microscopy. The complex plays a key role in destabilizing and unwinding duplex DNA during DNA replication. The team's findings provide new insights into the mechanism and function of the MCM2-7 complex.
Researchers discovered that bacteria time their sporulation decision with their cell-division cycle, using the location of genes on the circular chromosome. This timing allows for accurate determination of whether to reproduce or form spores.
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.
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 at Argonne National Laboratory have gained a clearer understanding of the origin recognition complex (ORC), a protein complex that directs DNA replication. The crystal structure shows how ORC's main body has five subunits, including one that protrudes from the core to contact another subunit.
A new study by Lomonosov Moscow State University researchers clarifies the DNA alarm-system, which detects single-strand breaks and activates kinase ATM to signal repair. This system prevents cancer-causing mutations and cell death.
Researchers develop a technique to label and track new DNA pieces, revealing hotspots for genetic flaws. These sites are crucial regulatory switches that can lead to genetic diseases or cancer.
Researchers have identified widespread incorporation of ribonucleotides in genomic DNA, with hotspots found in nuclear and mitochondrial DNA. The Ribose-seq technique allows for the precise location of ribonucleotides, which can affect genome stability and function.
A new study from Harvard Medical School reveals that genetic variants control DNA replication timing, varying among people. This variation affects mutation rates and individual disease risk, including blood cancers.
A Whitehead Institute team found that protein SUUR acts to control gene copy number by moving along with the engine of the train, acting like a brakeman to stall or derail it. This finding sheds light on fragile genomic regions associated with chromosomal abnormalities and raises questions about its function and regulation.
Researchers pinpoint key moments in the beginning of DNA replication, including structural details about the enzyme that unwinds the DNA double helix. The study's findings offer insights into how the enzyme becomes reactivated to begin its work splitting the DNA.
Researchers identify two critical controls that tie DNA replication to cell division in bacteria, enabling them to enter a 'zombie-like' state when blocked. This discovery opens doors to developing new drugs that target the bacterial cell cycle to combat infections.
A team of researchers has identified a unique molecular mechanism involved in DNA duplication during cell division, revealing how a key enzyme governs DNA through a gated system. The study suggests a route for stopping cell division in diseases like cancer by controlling the entry point of the helicase onto DNA.
Researchers at Rockefeller University developed the first model system to understand the DNA 'replication fork' process in eukaryotic cells. This breakthrough enables scientists to study the molecular tools involved in cell division and may have significant implications for human disease research, particularly cancer.
Researchers found that an enzyme thought to reside only in mitochondria can also produce acetyl-CoA in the nucleus, leading to faster cancer cell growth. The discovery may have broader implications for understanding epigenetic regulation in various physiological and pathological conditions.
The modENCODE Project has provided new genomic advances on embryonic development, DNA replication, and transcriptional regulation. Researchers compared developmental gene expression between Drosophila melanogaster and Caenorhabditis elegans, finding conserved gene expression patterns during development, despite significant differences ...
Researchers at Scripps Research Institute engineered a bacterium to replicate unnatural DNA bases, which could lead to breakthroughs in medicine, nanotechnology, and protein therapeutics. The unique organism can contain three pairs of DNA bases instead of the traditional two, providing new possibilities for genetic coding.
A team of researchers has discovered a cellular factor called Rif1 that regulates the timing of DNA replication, ensuring proper cell division and preventing tumor formation. The study suggests that Rif1 prevents 'DNA replication stress', a process causing genome instability.
Researchers from Curtin University found natural radioactivity in DNA can alter molecular structures, creating new molecules that do not belong to the four-letter alphabet of DNA. This could lead to genetic mutations by confusing DNA replication mechanisms.
Researchers have unveiled a biological process that explains how DNA can be damaged during genome replication, which relies on protein RPA. Cells use this protein as 'band aids' to protect DNA temporarily during replication, but if they run out, DNA breaks severely and cells cannot divide.
Researchers have discovered the human enzyme PrimPol, which recognises and repairs DNA lesions during replication, preventing breaks in chromosomes. This ancient enzyme has been found in archaebacteria and is thought to have played a key role in genome evolution and cancer development.
Researchers at the University of Nottingham have found a type of archaea that can reproduce without normal replication processes, growing faster in its absence. This discovery challenges existing understanding of DNA replication and has implications for cancer research.
Scientists have found a unique DNA repair mechanism that leads to increased genetic mutations, potentially contributing to tumor formation and cancer. This 'desperation replication' triggers bursts of genetic instability and can occur in non-dividing cells, making it a potential route for cancer formation.
Researchers discovered a unique DNA repair mechanism that utilizes a 'desperation strategy' to patch breaks in chromosomes. This process, called break-induced replication, can lead to increased mutagenesis and potentially drive cancer formation.
Researchers have captured a key step in the molecular 'dance' necessary for cell division by imaging the enzyme that unwinds DNA double helices. The study reveals how this enzyme recruits and interacts with the origin recognition complex, enhancing understanding of essential biological processes.
Researchers discovered that abnormal histone protein modification impairs DNA repair machinery, leading to a potential new way of detecting colorectal cancers. The study, published in Cell, reveals a novel mechanism explaining the root cause of some forms of colorectal cancers.
CNIO researchers have successfully mapped the proteins involved in human DNA replication, a process targeted by many chemotherapeutic agents. The study provides new insights into the mechanisms underlying cancer cell division and holds promise for developing new therapeutic strategies.
Researchers found that ATRX deficiency leads to increased DNA damage and telomere dysfunction. Mice lacking neural ATRX exhibited systemic endocrine dysfunction and shortened lifespans, mirroring human premature aging disorders.
For the first time, scientists have demystified a key step in human DNA replication by discovering how a sliding clamp loads onto DNA. The research reveals that a clamp loader quickly removes the clamp from DNA when polymerase is absent, allowing the polymerase to capture and complete the assembly of the holoenzyme.
Scientists have discovered two structural apparatuses that collaborate to protect repetitive DNA during replication. Disrupting both heterochromatin and replication fork proteins increases abnormal chromosomes and cell death.
A Johns Hopkins research team has identified a protein called HIF-1α that helps cells slow down their growth in response to low oxygen levels. This process can potentially be used to treat diseases such as cancer and other conditions where cell growth is uncontrolled.
A team of scientists has discovered quadruple helix DNA structures in human cells, which may be a new target for cancer treatment. The discovery was made using fluorescent biomarkers and shows clear links between quadruplexes and DNA replication.
Researchers found that certain 'checkpoint mutants' ignore the normal signal to stop replicating DNA after losing nucleotides, instead continuing to unwind and create damaged DNA strands.
A Thomas Jefferson University team found that histone-modifying proteins, such as TrxG and PcG, remain attached to DNA after replication, rather than histones. This challenges the longstanding paradigm of epigenetic marks and has significant implications for understanding gene expression and disease mechanisms.
Scientists at Scripps Research Institute discover that unnatural DNA bases can replicate efficiently, suggesting an expanded genetic alphabet could carry more information. The finding has implications for the origins of life and the development of novel molecular tools.
A DNA replication protein called Cdt1 is involved in both DNA replication and mitosis, a later step of the cell cycle. This discovery provides a possible explanation for why many cancers have genomic instability and an abnormal number of chromosomes.
Researchers have mapped the molecular-level details of how protein machinery binds and wraps DNA to start replication, a crucial process for cell division. The study sheds light on how this complex choreography is orchestrated by intricate cellular proteins, potentially leading to new ways to fight cancer.
Researchers have solved part of the mystery of DNA mismatch repair (MMR) in eukaryotes, revealing a brief window of opportunity for MMR proteins to identify new DNA strands. This discovery sheds light on how eukaryotes eliminate genetic errors and develop cancer resistance.