Hepatitis B virus (HBV) is a major global health concern, affecting millions of people worldwide. HBV is part of the hepadnaviridae family and one of the primary causes of acute and chronic liver infections, leading to conditions such as cirrhosis and hepatocellular carcinoma (HCC). Understanding the intracellular transport and genome repair mechanisms of HBV is crucial for developing new drugs, which-in combination with immune modulators-may contribute to potential cures. This review will explore the current knowledge of HBV intracytoplasmic and nuclear transport, as well as genome repair processes, while drawing comparisons to other viruses with nuclear replication.
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State Key Laboratory of Wheat Improvement, School of Advanced Agricultural Sciences, Peking University, Beijing 100871, China; Beijing Life Science Academy, Beijing 102299, China. Electronic address:
It has been hypothesized that DNA damage has the potential to induce DNA hypermethylation, contributing to carcinogenesis in mammals. However, there is no sufficient evidence to support that DNA damage can cause genome-wide DNA hypermethylation. Here, we demonstrated that DNA single-strand breaks with 3'-blocked ends (DNA 3'-blocks) can not only reinforce DNA methylation at normally methylated loci but also can induce DNA methylation at normally nonmethylated loci in plants.
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Gene Regulation Laboratory, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, OX3 9DS, Oxford, UK.
Individual enhancers are defined as short genomic regulatory elements, bound by transcription factors, and able to activate cell-specific gene expression at a distance, in an orientation-independent manner. Within mammalian genomes, enhancer-like elements may be found individually or within clusters referred to as locus control regions or super-enhancers (SEs). While these behave similarly to individual enhancers with respect to cell specificity, distribution and distance, their orientation-dependence has not been formally tested.
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Robson DNA Science Centre, Charbonneau Cancer Institute, Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
To tolerate oxidative stress, cells enable DNA repair responses often sensitive to poly(ADP-ribose) (PAR) polymerase 1 and 2 (PARP1/2) inhibition-an intervention effective against cancers lacking BRCA1/2. Here, we demonstrate that mutating the CHD6 chromatin remodeler sensitizes cells to PARP1/2 inhibitors in a manner distinct from BRCA1, and that CHD6 recruitment to DNA damage requires cooperation between PAR- and DNA-binding domains essential for nucleosome sliding activity. CHD6 displays direct PAR-binding, interacts with PARP-1 and other PAR-associated proteins, and combined DNA- and PAR-binding loss eliminates CHD6 relocalization to DNA damage.
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Cecropin AD (CAD), a hybrid antimicrobial peptide composed of the first 11 residues of cecropin A and last 26 residues of cecropin D, is a promising antibiotic candidate. Therefore, an efficient and convenient method for producing CAD is necessary for commercial applications. The Newcastle disease virus (NDV) has been widely used as a platform for gene delivery and exogenous protein expression.
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ART and Reproductive Biology Laboratory, University Hospital and School of Medicine, Picardie University Jules Verne, CHU Sud, 80000 Amiens, France.
Today, accumulating evidence highlights the impact of oxidative stress (OS) on semen quality. It is considered to be a key factor contributing to the decline in male fertility. OS is detected in 30-80% of men with infertility, highlighting its strong association with impaired reproductive function and with clinical outcomes following the use of assisted reproductive technologies.
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