Articles tagged with Dna Repair
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A Goethe University-led study reveals how mutations in the SPRTN enzyme cause chronic inflammation and premature ageing. The research team found that damaged DNA in the cell nucleus leaks into the cytoplasm, activating defense mechanisms and leading to chronic inflammation.
A machine-learning-based algorithm developed by Tokyo Metropolitan University researchers can accurately count sister chromatid exchanges (SCEs) in chromosomes, giving a more objective measurement. The accuracy rate is 84%, which could help diagnose disorders like Bloom syndrome with greater consistency.
Researchers discovered that certain cancers rely on an emergency DNA repair mechanism called break-induced replication to survive. By understanding how this mechanism works, scientists can develop targeted therapies to selectively kill cancer cells while leaving normal cells intact.
Scientists have developed an experimental drug called TY1 that repairs DNA damage and promotes healing in damaged tissue. The breakthrough could lead to new treatments for heart attacks, autoimmune diseases, and other conditions.
Researchers at the University of Texas M. D. Anderson Cancer Center discovered that inflexible DNA within nucleosomes regulates the positioning of INO80, a chromatin remodeling complex. This unique mechanism allows INO80 to position itself on the surface of nucleosomes at the right location.
Researchers have discovered a new class of BRCA1 mutations that can be targeted by HSP90 inhibitors, potentially improving treatment outcomes for patients with breast cancer. The study found that these mutations are more resistant to PARP inhibitor treatment but can be overcome with low-dose HSP90 inhibition.
A new type of DNA damage, glutathionylated DNA adducts, accumulates at high levels in mitochondrial DNA, affecting energy production and stress response. The discovery sheds light on how cells sense and respond to stress, with potential implications for diseases like cancer and diabetes.
A team of scientists has found that Dicer, an ancient protein, plays a vital role in resolving conflicts between transcription and replication processes in the genome. Without Dicer, T-R collisions lead to DNA damage, mutations, and cancer. The study highlights the importance of Dicer in maintaining genome stability.
Researchers used CRISPR technology to identify HMGN1, a nuclear binding protein that contributes to trisomy 21-related CHDs. The study found that an overabundance of HMGN1 leads to abnormal heart development and gene expression.
Researchers identified a previously unknown gene, SMARCAL1, that increases the risk of developing osteosarcoma in children and young adults. The study found that approximately 2.6% of children with osteosarcoma carry inherited mutations in SMARCAL1, which may weaken DNA repair and promote tumor growth.
Telomeres, which cap chromosomes, are inherited from parents in a parent-of-origin effect, with mothers contributing short telomeres and fathers long ones. This process is linked to cancer risk and aging, and researchers hope to study it further using human genome sequencing.
Researchers at CNIO have created a 'human repairome', a catalogue of 20,000 DNA 'scars' that reveal how genes affect DNA repair. This information can help determine the best treatment for each cancer type and overcome resistance to therapy.
Researchers found that mutations in the CFAP410 gene change its interaction with another protein, making motor neuron cells more vulnerable to DNA damage and cell death. This discovery provides new insights into the mechanisms underlying Motor Neurone Disease and highlights potential targets for new therapies.
A recent study by researchers at The University of Osaka discovered the crucial role of DNA repair enzyme Polβ in safeguarding the developing brain from harmful mutations. Accumulation of indel mutations near CpG sites may contribute to neurodevelopmental disorders.
Researchers found that Fen1 protein improves cell tolerance to alovudine by counteracting the toxic effect of 53BP1. This discovery promises new cancer treatments and biomarkers for cancerous cells with Fen1 deficiency.
Scientists have found that nucleosomes act as gatekeepers for p53's molecular partners, controlling its access to the genetic code. This discovery reveals a new layer of regulation over p53's activity and opens possibilities for developing cancer therapies that restore or control p53 function.
Researchers developed a chemical probe that binds to damaged mitochondrial DNA, blocking enzymatic processes that lead to its degradation. This approach lessens mtDNA loss, preserving energy production in vulnerable tissues. The new molecule successfully reduced inflammation and maintained functional DNA despite chemical tagging.
The Association for Molecular Pathology publishes guidelines for detecting homologous recombination deficiency (HRD) in cancer. The report includes recommendations for clinical laboratories, addressing technical aspects of genomic instability and HRD analysis.
Researchers at MD Anderson have made significant progress in treating non-small cell lung cancer (NSCLC) by combining chemotherapy, immunotherapy, and surgery. They found that pre-surgical combination therapy showed promising results, with high rates of pathological complete response and major pathological response.
Researchers found that cigarette smoke and reduced DNA repair capacity combine to increase cancer risk, with normal lung cells showing extensive damage after smoke exposure. The study's findings support a 'double hit' model, highlighting the critical role of XPC protein in preventing DNA damage.
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.
Scientists at MIT have identified new potential targets for treating Alzheimer's disease, including a pathway involved in DNA damage repair. The study suggests that a combination of treatments targeting different cellular pathways may be more effective in blocking disease progression.
Researchers have elucidated the molecular mechanism by which LEM-3 cuts DNA bridges during cytokinesis, a crucial step in cell division. The study found that LEM-3 is essential for resolving persistent DNA bridges and maintaining chromosomal stability.
Researchers at Northwestern University discovered that DNA's behavior changes in a crowded environment, affecting the amount of stress required for strand separation. The study used microscopic magnetic tweezers to investigate interactions between DNA and various molecules.
The treatment demonstrated early signals of efficacy, with 65.7% of patients experiencing lasting stable disease, and was generally well-tolerated, with most adverse events being mild and manageable.
Scientists at the University of Birmingham have made strides in understanding how cells repair DNA damage. Two studies identify key players and mechanisms involved in preventing excessive DNA signal overload, which could lead to refinements in future cancer therapies.
A University of Iowa-led study has revealed the unexpected structure adopted by the DNA repair protein RAD52 as it binds and protects replicating DNA in dividing cells. This understanding may help researchers develop new anti-cancer drugs targeting RAD52.
Senescent cells can cause chronic inflammation through the secretion of inflammatory molecules, leading to age-related diseases. The study found that a cellular circuit controlling DNA repair can suppress this inflammation, offering potential ways to promote healthier aging.
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.
A new study reveals that radiotherapy has opposite effects on glioblastoma multiforme (GBM) and low-grade gliomas (LGG), with GBM patients living longer after treatment. The study highlights the need for personalized treatment approaches based on genetic and molecular characteristics to improve survival outcomes.
Researchers at Scripps Research have captured the first detailed images of polymerase theta (Pol-theta) in action, revealing its molecular processes responsible for a range of cancers. The study provides a blueprint for designing more effective cancer drugs by understanding how Pol-theta repairs DNA using a two-step process.
Research suggests that APOBEC enzymes, which normally target viruses, are unusually active in the brains of Huntington’s patients and cause genetic changes. The study found that APOBEC3A was most pronounced in causing DNA repeat expansion in a CAG/CTG tract.
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.
Engineers at USC Viterbi School of Engineering have developed a new CRISPR toolkit that allows for precise, remote-controlled genome editing using focused ultrasound. This breakthrough enables the treatment of various genetic disorders and diseases by activating or silencing specific genes with precision.
Researchers at the Hubrecht Institute have mapped the activity of DNA repair proteins in individual human cells, discovering unique and sometimes rare ways to repair DNA damage. These proteins organize into 'hubs' where multiple damaged DNA regions come together, making the process more efficient.
Researchers have uncovered a mechanism by which the BRCA1 gene influences fertility, leading to genetic errors that can cause infertility. This breakthrough discovery enables potential therapeutic avenues for correcting or treating fertility issues in BRCA1 patients.
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 at Colorado State University have identified an alternate method to study changes during the DNA replication process in lab settings using genetically modified yeast. This new approach provides a less toxic and quickly reversible alternative to hydroxyurea, allowing for better insight into cell cycle arrest mechanisms.
A new mechanism of DNA damage response has been identified, involving an RNA transcript that regulates genome stability. The study found that NEAT1, a long non-coding RNA transcript, plays a crucial role in recognizing and repairing DNA double-strand breaks.
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.