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A recent study conducted at the University of California Los Angeles (UCLA) focused on the mutability of specific regions within the thyA gene of Escherichia coli when exposed to the mutagen cisplatin. The research found that mutations occurred preferentially at certain 3 bp sequences within the gene, and that some premutational lesions were masked by repair mechanisms. The study utilized a novel reporter gene, tdk, to detect these mutations, highlighting the advantages of this detection system. This peer-reviewed research sheds light on the anatomy of cisplatin hotspots in the tdk gene of Escherichia coli, providing valuable insights into genetic mutations in bacteria. [Extracted from the article]

The article discusses the structure of human MUTYH, a DNA glycosylase involved in DNA repair, and the functional profiling of cancer-associated variants near its [4Fe-4S] cofactor. Most variations near the cofactor result in loss of enzyme activity, with some exceptions like R241Q and N238S. The study reveals an allosteric network between the cofactor and the active site that regulates DNA repair, suggesting a complex mechanism for MUTYH function. [Extracted from the article]

A recent study conducted at Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine focused on characterizing N6-methyladenosine long non-coding RNAs in sporadic congenital cataract (CC) and age-related cataract (ARC). The research identified differences in m6A modification patterns in lncRNAs between CC and ARC, with a higher level of m6A peaks in ARC compared to CC. The study also highlighted altered lncRNAs in ARC associated with intracellular organelles and nucleotide excision repair, providing new insights into the potential pathogenic mechanisms of CC and ARC. [Extracted from the article]

A recent study conducted by the Chinese Academy of Fishery Sciences in Guangzhou, China, focused on the dynamic deformylation of 5-formylcytosine and decarboxylation of 5-carboxylcytosine during the differentiation of mouse embryonic stem cells into mouse neurons. The research explored novel DNA demethylation pathways and their roles in regulating cell fate. The study found that deformylation and decarboxylation activities changed during the differentiation process, independent of DNA cytosine methyltransferases and ten-eleven translocation enzymes. This peer-reviewed research provides valuable insights into stem cell research and cell fate regulation. [Extracted from the article]

Researchers from Chengdu University of Traditional Chinese Medicine have published a report on the mechanisms for repairing sperm DNA damage, highlighting the impact of DNA damage on male infertility and adverse reproductive outcomes. The study emphasizes the importance of understanding DNA repair mechanisms during spermatogenesis, oocytes after fertilization, and early embryonic development stages. The research identifies nucleotide excision repair, base excision repair, mismatch repair, and double-strand break repair as key mechanisms for repairing sperm DNA damage, with proteins like XRCC4-like factor and PAXX playing critical roles in the process. This peer-reviewed study aims to provide a perspective for further research on DNA damage repair mechanisms in spermatozoa. [Extracted from the article]

Recent studies from the University of Newcastle focus on DNA damage in testicular germ cells and spermatozoa, exploring when and how it is induced, how to measure it, and its implications. The research highlights the importance of DNA integrity maintenance in male germ cells, the impact of paternal age on mutation rates, and strategies to manage high levels of DNA damage in spermatozoa for offspring health. This peer-reviewed research provides valuable insights into the genetic processes involved in male reproduction and offers potential implications for assisted conception. [Extracted from the article]

Research conducted at Southwest University in Chongqing, People's Republic of China, has developed a new method for monitoring base excision repair (BER) activity in cancer cells. The study introduces a highly reliable triple loop-interlocked DNA codec (GATED) that allows for precise assessment of BER activity through signal amplification mediated by multiple enzymes. This innovative tool could advance the understanding of DNA repair processes, cancer development, and treatment strategies by providing real-time monitoring of BER activity and enabling the screening of BER inhibitors in cancer cells. [Extracted from the article]

A study conducted at Wenzhou Medical University in China explored the role of FTX in promoting esophageal cancer progression and desensitizing cancer cells to radiation. The research found that up-regulated FTX in esophageal cancer patients is associated with poor clinical outcomes, and silencing FTX inhibits cancer cell growth and migration. The study concluded that FTX acts as a ceRNA to regulate the transcription of WEE1 and ERCC1 by sponging hsa-miR-99a/b-3p, contributing to the malignant biological phenotype of esophageal cancer cells. [Extracted from the article]

A recent study from Georgia State University delves into the molecular architecture and functional dynamics of the pre-incision complex in nucleotide excision repair (NER), a crucial process for genome integrity. By combining cryo-EM and XL-MS data with AlphaFold2 predictions, researchers constructed an integrative model of the NER pre-incision complex (PInC), shedding light on its assembly, global motions, and disease mutations. This research, published in Nature Communications, offers insights into the mechanisms underlying xeroderma pigmentosum and Cockayne syndrome. For more information, readers can access the full article for free at the provided link. [Extracted from the article]

A recent study conducted by researchers at the Van Andel Institute focused on chromatin and the human glycosylase OGG1 enzyme. The study found that OGG1 plays a crucial role in repairing oxidized DNA bases and is involved in various pathological conditions such as cancer and neurodegenerative diseases. The researchers used cryo-EM structures to examine how OGG1 operates on longer DNA and nucleosomes. They discovered that OGG1 preferentially binds near dsDNA ends at nucleosomal entry/exit sites and can also bend the nucleosomal entry DNA and bind to internal nucleosomal DNA sites. The study suggests that OGG1's DNA base search mechanism may be dependent on the chromatin context and that it may work in conjunction with chromatin remodelers to remove oxidized DNA bases. [Extracted from the article]

A recent study conducted by researchers from Charles River Laboratories International Inc. explores the role of polymerase b (POLB) in maintaining genomic stability through its dual functionality as a lyase and polymerase. The researchers developed a high-throughput mass spectrometry-based assay to measure the two distinct biochemical activities of POLB in a single assay. This assay allowed for the screening of 200,000 small molecules to identify potential modulators of POLB activity. The study demonstrates the flexibility of high-throughput mass spectrometry approaches in drug discovery and highlights the novel application of this technology in multiplexed high-throughput screening. [Extracted from the article]

Prostate cancer is a common cancer in men in the United States and Puerto Rico, with high mortality rates. Researchers at Ponce Health Sciences University conducted a pilot study to evaluate the DNA repair capacity (DRC) in Puerto Rican men with and without metastatic castration-resistant prostate cancer (mCRPC) using lymphocytes as surrogate markers. The study found significant differences in DRC between the control group and both the mCRPC and non-mCRPC groups. However, no significant differences were found between PCa cases stratified by disease aggressiveness. This research may contribute to improved patient diagnosis and stratification in terms of disease progression. [Extracted from the article]

A recent study conducted by researchers at the University of Georgia explores the biological factors involved in aflatoxin-induced DNA damage, which is a risk factor for liver cancer. The study used a method called tXR-seq to measure the repair of DNA adducts caused by aflatoxin at the single-nucleotide level. The results showed that transcription-coupled repair plays a significant role in the removal of DNA damage. Additionally, the study analyzed the distribution of repair sites within the 3D human genome organization and found that repair activity was higher in chromosomes positioned closer to the nuclear center and regions within A compartments. These findings provide insights into the complex relationship between DNA damage repair, transcription, and genome organization, shedding light on the mechanisms underlying aflatoxin-induced mutagenesis. [Extracted from the article]

Researchers at the University of Baghdad have conducted a study on the relationship between genetic polymorphisms of the ERCC2 gene and the risk of developing colorectal cancer (CRC). The study involved 121 participants, including 72 CRC patients and 49 healthy individuals. The researchers found that certain single nucleotide polymorphisms (SNPs) of the ERCC2 gene were associated with an increased or decreased risk of CRC. The study suggests that genetic polymorphisms of the ERCC2 gene can influence the susceptibility to CRC. [Extracted from the article]

A recent study conducted by researchers at Sun Yat-Sen University in China has provided insights into the molecular mechanisms and potential targets for human testicular aging. The study used single-cell RNA sequencing to analyze gene expression in testicular cells from young and old individuals. The findings revealed age-related changes in germline and somatic niche cells, including disruptions in DNA repair pathways and stress-related changes in somatic cells. The research suggests potential therapeutic targets for addressing age-related male fertility decline and hypogonadism. However, the study's sample size was limited, and further research is needed to fully understand the functional and mechanistic aspects of testicular aging. [Extracted from the article]

A recent report discusses research findings on bladder cancer from Comenius University. The study aimed to explore the prognostic value of proteins involved in nucleotide excision repair (NER) and translesion DNA synthesis (TLS) in muscle-infiltrating bladder carcinoma (MIBC) patients. The researchers found significant correlations between the tumor expression of certain proteins and inferior overall survival (OS), suggesting that these proteins could serve as prognostic biomarkers and potential therapeutic targets in MIBC. However, further validation through a prospective trial is needed. [Extracted from the article]

A new report discusses research findings on solid cancer from Johns Hopkins University in Baltimore, Maryland. The study focuses on the MUTYH gene, which is associated with colorectal cancer and other cancers. The researchers analyzed data from over 350,000 solid tumor biopsies and found that biallelic germline pathogenic MUTYH variants were present in 119 tissue biopsies, mostly colorectal cancers. They also identified germline heterozygous pathogenic variants in 5,991 biopsies, with some cancer types showing somatic loss of heterozygosity for MUTYH and defective base excision repair. The researchers concluded that while the effect is modest, further studies are needed to confirm these findings. [Extracted from the article]

A new study conducted at the University of California Los Angeles (UCLA) has examined the relative binding affinity of several covalent polycyclic aromatic hydrocarbon (PAH)-DNA adducts at a mutational hotspot implicated in cancer risk. The study found that certain PAHs have greater binding affinity than the known carcinogen benzo[a]pyrene (B[a]P), and these PAH-DNA adducts may resist repair mechanisms, contributing to their genotoxic potential. The research suggests that the study of PAH genotoxicity needs to be expanded, with implications for public policy and the health sciences. The study's findings can be applied to assess the genotoxicity of other unclassified compounds. [Extracted from the article]

A recent report from the University of Toronto discusses research on immunoglobulins and their role in humoral immunity. The study focuses on the protein FAM72A, which downregulates the base excision repair protein UNG2, allowing for the persistence of deoxyuridine (dU) mutations that initiate somatic hypermutation and class switch recombination. The researchers discovered that FAM72A recruits a C-terminal to LisH (CTLH) E3 ligase complex to target UNG2 for degradation. Deficiency in CTLH complex components leads to elevated UNG2 levels and reduced somatic hypermutation and class switch recombination. The study suggests that FAM72A plays a critical role in both humoral immunity and cancer development. [Extracted from the article]

A recent study conducted by researchers at the University of Belgrade in Serbia has highlighted the effectiveness of the Comet assay in detecting DNA damage at the cellular level. The Comet assay is a rapid and highly sensitive method that can detect single-stranded and double-stranded DNA breaks, incomplete excision repair, and cross-linking sites. It is applicable to both proliferating and non-proliferating cells and can be used with all types of eukaryotic cells. The assay has several advantages, including its sensitivity, versatility, speed, and broad applicability, making it a valuable tool in various scientific and clinical fields for assessing DNA damage. [Extracted from the article]

A recent study conducted by researchers at Hebrew University of Jerusalem explores the coordination of transcription-coupled repair (TCR) and repair-independent release of lesion-stalled RNA polymerase II (Pol II). The study reveals that the p97-proteasome pathway can evict lesion-stalled Pol II independently of repair, and both TCR and repair-independent eviction require CSA and ubiquitination. The research sheds light on the fate of lesion-stalled Pol II and may provide insights into the molecular basis of genetic diseases caused by defects in TCR genes. The full article can be accessed for free at the Nature Communications website. [Extracted from the article]

Researchers from Nanjing Medical University in China have conducted a bioinformatics analysis to explore the role of the Excision Repair Cross-Complementation (ERCC) family of genes in cancer. They found that variations in ERCC gene expression were associated with patient prognosis and the tumor microenvironment in multiple cancer types. Additionally, they validated the role of ERCC2 in bladder cancer through in vitro assays, which showed that knockdown of ERCC2 inhibited the proliferation, migration, and invasion of bladder cancer cells. The researchers believe that the ERCC family of genes could be a potential target for cancer treatment. [Extracted from the article]

A recent study conducted by researchers from the University of Massachusetts in Amherst focuses on Listeria monocytogenes, a potentially fatal foodborne pathogen commonly found in food processing facilities. The study explores the resistance of L. monocytogenes to benzalkonium chloride (BAC), a widely used sanitizer. Through chemical mutagenesis, the researchers identified two mutants with increased tolerance to BAC and found that they also displayed increased resistance to fluoroquinolone antibiotics. The study provides insights into alternative mechanisms for increased BAC tolerance and contributes to our understanding of how L. monocytogenes persists in the food processing environment. [Extracted from the article]

A recent study conducted by researchers at Prince of Songkla University examined the relationship between the expression of certain proteins and the response to platinum-based chemotherapy in patients with epithelial ovarian cancer. The study found that low expression of the protein BRCA1 was associated with a good response to chemotherapy and favorable overall survival. Additionally, the study suggested that combined low expression of PARP1/BRCA1 and ERCC1/BRCA1 may enhance the response to treatment. The findings provide evidence for potential therapeutic strategies in ovarian cancer treatment, although further research is needed. [Extracted from the article]

A recent study conducted by researchers at Yeditepe University in Istanbul, Turkey, explored the role of two genes involved in DNA repair mechanisms, Xeroderma Pigmentosum Complementation Group C (XPC) and DNA Damage Binding Protein 2 (DDB2), in ovarian cancer susceptibility. The study found that individuals with certain variations in these genes had a reduced likelihood of developing ovarian cancer, while others faced an elevated risk. These findings highlight the importance of DNA repair systems in the development of ovarian cancer and suggest the potential for tailored treatment strategies based on genetic factors. Further research in larger and more diverse populations is needed to validate these findings. [Extracted from the article]

A study conducted at Tsinghua University has shed light on the mechanisms by which bacteria develop antibiotic resistance through mutagenesis. The researchers found that ribosome-targeting antibiotics, such as gentamicin, cause genome-wide premature stalling of RNA polymerase, leading to lesions in the DNA and subsequent mutations. This process occurs shortly after antibiotic exposure, allowing resistance to rapidly emerge in the bacterial population. The findings provide insights into the action of ribosomal antibiotics and suggest new strategies for combating resistance. [Extracted from the article]

Researchers at the University of North Carolina have conducted a genome-wide analysis of transcription-coupled repair (TCR) in the model organism Caenorhabditis elegans. TCR is a mechanism by which bulky DNA adducts are removed from the genomes of multicellular organisms. The study used eXcision Repair-sequencing (XR-seq) to map repair events in wild-type strains with normal excision repair, strains lacking TCR, and strains that only repair by TCR. The analysis revealed previously unrecognized sites of transcription and enhanced understanding of the genome of Caenorhabditis elegans. The research was supported by the National Institutes of Health. [Extracted from the article]

According to a preprint abstract from biorxiv.org, researchers investigated the clastogenicity and mutagenicity of benzo[b]fluoranthene (BbF), a common environmental pollutant, in mice after a 28-day oral exposure. The study found that BbF caused dose-dependent increases in chromosome damage and mutation frequencies in bone marrow and liver. The mutation spectrum of BbF was similar to that of benzo[a]pyrene, another mutagenic pollutant. The research highlights the usefulness of duplex sequencing for assessing the mutagenicity of environmental pollutants. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent study conducted by the CSIR - Indian Institute of Chemical Biology 4 in West Bengal, India, has found that DNA abasic sites can be targeted to enhance the response to the cancer treatment drug temozolomide (TMZ). The study showed that increasing concentrations of TMZ led to an accumulation of DNA abasic sites, which can be targeted by amino-quinoxaline small molecules (RA-1) to enhance the drug's effectiveness. The combination of TMZ and RA-1 resulted in a synergistic effect on both mismatch-repair (MMR)-proficient and deficient cancer cells, leading to DNA double-strand breaks and apoptosis. These findings provide a promising approach to improve the therapeutic response to TMZ in cancer treatment. [Extracted from the article]

A recent research study conducted by the Department of Pathology has identified the excision repair cross-complementation group 3 gene (ERCC3) as a breast cancer susceptibility gene. The study analyzed genetic data from 291 breast cancer patients and 291 controls in mainland China. The researchers found a novel ERCC3 mutation in a breast cancer family and observed a negative association between ERCC3 expression and certain characteristics of breast cancer. The study suggests that the ERCC3 gene may increase breast cancer risk in the Han-Chinese population and could serve as a biomarker for the pathological diagnosis of breast cancer. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the impact of bioenergetic stress on antimicrobial resistance (AMR) and persistence. The study used a synthetic biology approach to examine the effects of increased ATP utilization on antibiotic efficacy in Escherichia coli. The researchers found that bioenergetic stress enhances ROS production, mutagenic break repair, and transcription-coupled repair, leading to the evolution of AMR. Additionally, bioenergetic stress potentiates antimicrobial persistence through stringent response activation. The findings have important implications for preventing the spread of AMR infections. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A recent study conducted by researchers at Tianjin Medical University General Hospital explores a potential treatment strategy for anaplastic thyroid carcinoma (ATC), a rare and aggressive form of thyroid cancer. The study focuses on the use of a glutathione-responsive abasic site trapping agent, which selectively targets ATC cells by inhibiting DNA repair processes. In vitro experiments demonstrate the agent's cytotoxicity towards ATC cells, while in vivo experiments show promising therapeutic effects on subcutaneous tumors. This research offers a new targeted chemotherapy approach for ATC with high selectivity and reduced adverse effects. [Extracted from the article]

A recent report from the Polish Academy of Sciences discusses the effects of kynurenic acid (KYNA) on the enzymatic activity of the DNA base excision repair pathway in specific areas of the sheep brain. The study found that increased levels of KYNA positively influenced the mRNA expression of certain enzymes involved in DNA repair and enhanced their efficiency in removing damaged nucleobases. The research suggests that KYNA may have a protective effect on genetic material in nerve and glial cells by stimulating the expression and efficiency of these enzymes. Further research is needed to fully understand the implications of these findings. [Extracted from the article]

A recent preprint abstract discusses the coordination of transcription-coupled repair (TCR) and repair-independent release of stalled RNA polymerase II (PolII) in response to transcription-blocking lesions (TBLs). The study utilized Protein-Associated DNA Damage Sequencing (PADD-seq) and found that the p97-proteasome pathway can evict lesion-stalled PolII independently of repair. Both TCR and repair-independent eviction require CSA and ubiquitination. The study provides insights into the fate of lesion-stalled PolII and may contribute to understanding genetic diseases caused by defects in TCR genes. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

This document is a patent for methods, compositions, and devices for treating cancer with illudofulvenes. The patent describes a method for using an acylfulvene compound to treat a cancerous tumor in a patient. The method involves determining the enhanced expression of a MYC biomarker and the attenuated expression of a TCR biomarker in the tumor. If these conditions are met, the patient is treated with an effective amount of the acylfulvene compound. The patent also includes additional claims and can be accessed for further information. [Extracted from the article]

Researchers at Vanderbilt University have reported findings on DNA repair enzymes, specifically focusing on endonuclease VIII-like 3 (NEIL3). NEIL3 is a versatile DNA glycosylase that repairs various chemical modifications to DNA. Unlike other glycosylases, NEIL3 has a preference for lesions within single-strand DNA and at single/double-strand DNA junctions. This research provides insight into NEIL3's biological functions, its role in disease, and its three-dimensional structure. The study was funded by the National Institutes of Health and the Vanderbilt Training Program in Environmental Toxicology. [Extracted from the article]

A recent study from Duke University in Durham, North Carolina, explores the role of transcription-coupled DNA repair in protecting genome stability when DNA strand breaks occur due to oxidative stress. The research highlights the importance of understanding how transcription is regulated during DNA repair and the role of RNA molecules in maintaining genome stability. The study provides an update on how cells protect transcribed genome loci through transcription-coupled repair pathways. This research was supported by the National Institutes of Health (NIH) in the United States and has been peer-reviewed. [Extracted from the article]

A recent study conducted by researchers at Baptist Health South Florida explored the efficacy and safety of the base excision repair inhibitor TRC102 in combination with temozolomide (TMZ) for patients with recurrent glioblastoma (GBM). The study involved a phase 2 clinical trial called BERT, which enrolled 19 bevacizumab-naive GBM patients at first recurrence. The primary endpoint of the trial was response rates, but objective responses were not observed, and a second arm of the trial was not opened. The study found that the combination therapy was safe and feasible for patients with recurrent GBM, and further evaluation of combination therapy in biomarker-enriched trials is warranted. [Extracted from the article]

A new report from the Siberian Branch of the Russian Academy of Sciences presents fresh data on amino acids. The research focuses on DNA polymerase b (Polb), which plays a crucial role in maintaining genome stability and repairing DNA. The study examines the effects of single-nucleotide polymorphisms (SNPs) in the POLB gene on the enzymatic properties of Polb. The researchers found that certain amino acid substitutions in Polb variants led to a decrease in polymerase activity, potentially contributing to an elevated level of unrepaired DNA damage. This research provides insights into the role of amino acids in DNA repair and their potential association with cancer. [Extracted from the article]

A recent study conducted by researchers at Maltepe University examined the levels of oxidatively-induced DNA damage and base excision repair (BER) mechanisms in individuals with bipolar disorder (BD) and their siblings. The study found that both individuals with BD and their unaffected siblings exhibited similar abnormalities in DNA damage and BER, suggesting a familial susceptibility to BD. The findings indicate that targeting the oxidatively-induced DNA damage and BER pathway could be a promising therapeutic strategy for reducing the risk of age-related diseases and comorbidities in individuals with a genetic predisposition to BD. [Extracted from the article]

According to a preprint abstract, researchers have discovered that the interaction between mammalian Uracil DNA glycosylase (UNG) and replication protein A (RPA) determines whether uracil repair is high-fidelity or mutagenic. UNG removes uracils and initiates high-fidelity base excision repair, but during B cell development, activation-induced cytidine deaminase (AID) creates uracils that UNG processes in an error-prone manner for immunoglobulin somatic hypermutation or class switch recombination. The B cell tropic gammaherpesvirus (GHV) encodes a functional homolog of UNG, but it does not support hypermutation, suggesting that UNG's intrinsic properties influence repair outcome. This research has implications for mutagenesis in B cells and deamination-associated mutational signatures in cancer. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent report from the University of Connecticut discusses the formation, replication, and repair of tandem DNA lesions caused by ionizing radiation and radicals. These complex DNA damages are resistant to traditional repair methods and can block DNA replication, potentially leading to errors and contributing to aging, neurological diseases, and cancer. The research highlights the importance of understanding these lesions and developing effective repair strategies. The study was supported by the National Institute of Health and can be accessed for free through the journal DNA. [Extracted from the article]

A recent report from the University of Maryland explores the dysregulation of base excision repair (BER) factors in head and neck squamous carcinoma (HNSCC) and its implications for immunotherapy. The study found that BER genes are frequently overexpressed in HNSCC tumors, leading to increased mutation count and low infiltration of immune cells. Additionally, dysregulated BER factors in Human papillomavirus (HPV) positive tumors were associated with better overall survival. The researchers suggest that targeting the dysregulation of BER genes could serve as a potential prognosis marker and a target for immune checkpoint blockade in HNSCC cancers. However, further experimental validation is needed. [Extracted from the article]

A recent study published in Environmental and Molecular Mutagenesis focuses on genome integrity mechanisms and their importance for basic and environmental health sciences. The study includes research articles, reviews, and brief research communications that highlight cutting-edge findings and perspectives on DNA repair mechanisms. The research provides an updated understanding of enzymes involved in DNA repair and the impact of DNA damage and mutations caused by environmental mutagens. The study is dedicated to the legacy of Dr. Samuel H. Wilson. Financial support for the research was provided by various organizations, including the National Institutes of Health and the National Science Foundation. [Extracted from the article]

Researchers at St. Louis University have conducted a study on nucleotide excision repair (NER), a process that removes bulky DNA adducts caused by external factors like ultraviolet light. Defects in NER enzymes are associated with conditions such as Xeroderma Pigmentosum, trichothiodystrophy, and Cockayne syndrome. The researchers used a fluorescence enhancement technique to investigate the dynamics of the Xeroderma Pigmentosum group A protein (XPA) binding to DNA during NER. They successfully generated a fluorescent XPA protein (XPACy3) that maintained its DNA binding activity and exhibited a significant change in fluorescence upon binding to DNA. The study provides detailed methods for generating XPACy3 and maintaining its stability during biochemical and biophysical studies. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of deoxyuridine-rich cytoplasmic DNA in inhibiting immune responses and sensitizing resistant tumors to anti-PD-L1 therapy. The study found that inhibitors of the DNA damage response kinase ATR induce the incorporation of deoxyuridine (dU) by DNA polymerases, which is associated with the induction of interferons (IFN-1) and the potentiation of immune checkpoint inhibitors. The research also revealed that uracil DNA glycosylase (UNG)-initiated base excision repair and STING are required for ATRi-induced IFN-1 responses. Additionally, the study showed that UNG-deficient tumors have an increased response to immune checkpoint inhibitors. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of TRIP12, an E3 ligase, in DNA repair pathways. The study found that TRIP12 controls the levels and chromatin loading of DNA polymerase β (Polβ), which is crucial for base excision repair (BER). Excessive shuttling of Polβ by TRIP12 affects double strand break (DSB) formation and radiation sensitivity, highlighting its importance in BER. This research provides insights into the trafficking function of TRIP12 in DNA repair signaling pathways and its optimization of DNA repair pathway choice at complex lesion sites. Please note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent study conducted by researchers at the Department of Sciences and Technology in Taguig, Philippines, explores potential treatment strategies for African Swine Fever Virus (ASFV). ASFV is a significant threat to the pork industry, causing economic losses and concerns about food security. The study focuses on the identification of antiviral compounds from medicinal fungal metabolites that target specific proteins involved in the base excision repair pathway of ASFV. Through computer-aided drug discovery techniques, the researchers identified several lead candidates that show promise as potential antiviral drugs against ASFV. Further in vitro and in vivo studies are recommended to validate these findings. [Extracted from the article]

A recent preprint abstract discusses a study on transcription-coupled repair (TCR) in the model organism Caenorhabditis elegans. TCR is a mechanism that removes bulky DNA adducts induced by ultraviolet light. The study used eXcision Repair-sequencing (XR-seq) to generate genome-wide repair maps in wild-type strains with normal excision repair, strains lacking TCR, and strains that only repair by TCR. The analysis of these repair maps revealed previously unrecognized sites of transcription, providing new insights into the genome of Caenorhabditis elegans. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

A recent study has found that quinoline-based compounds have the potential to inhibit various enzymes that act on DNA. These compounds show inhibitory potency against both human DNMT1 and Clostridioides difficile CamA, which are involved in DNA methylation. The study also reveals that some of these compounds can inhibit other enzymes that act on DNA, such as polymerases and base excision repair glycosylases. Additionally, one of the compounds, known as compound 11, has been found to elicit a DNA damage response in cancer cells through p53 activation. However, it is important to note that this study has not yet undergone peer review. [Extracted from the article]