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Filename: controllers/Detail.php
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Function: _error_handler
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Function: require_once
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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Function: str_replace
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Werner syndrome (WS) is a disorder characterized by features of premature aging and increased cancer that is caused by loss of the RecQ helicase WRN. Telomeres consisting of duplex TTAGGG repeats in humans protect chromosome ends and sustain cellular proliferation. WRN prevents the loss of telomeres replicated from the G-rich strand, which can form secondary G-quadruplex (G4) structures. Here, we dissected WRN roles in the replication of telomeric sequences by examining factors inherent to telomeric repeats, such as G4 DNA, independently from other factors at chromosome ends that can also impede replication. For this we used the supF shuttle vector (SV) mutagenesis assay. We demonstrate that SVs with [TTAGGG]6 sequences are stably replicated in human cells, and that the repeats suppress the frequency of large deletions despite G4 folding potential. WRN depletion increased the supF mutant frequency for both the telomeric and non-telomeric SVs, compared with the control cells, but this increase was much greater (27-fold) for telomeric SVs. The higher SV mutant frequencies in WRN-deficient cells were primarily due to an increase in large sequence deletions and rearrangements. However, WRN depletion caused a more dramatic increase in deletions and rearrangements arising within the telomeric SV (70-fold), compared with non-telomeric SV (8-fold). Our results indicate that WRN prevents large deletions and rearrangements during replication, and that this role is particularly important in templates with telomeric sequence. This provides a possible explanation for increased telomere loss in WS cells.
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http://dx.doi.org/10.4161/cc.21399 | DOI Listing |
Int J Biol Macromol
December 2024
Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, PR China; Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, PR China. Electronic address:
Infectious Bursal Disease Virus (IBDV), a double-stranded RNA virus of the Avibirnavirus genus, causes significant vaccine failures in immunocompromised young poultry. The VP1 protein of IBDV undergoes post-translational modifications that are critical for viral RNA transcription, genome replication, and overall viral proliferation. Phosphorylation enhances the ability of the IBDV polymerase VP1 and facilitates viral replication, while the specific mechanisms underlying VP1 phosphorylation and its role in the IBDV life cycle remain largely unexplored.
View Article and Find Full Text PDFVet J
December 2024
College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China. Electronic address:
Immunoglobulins are important components of humoral immunity and play a crucial role in protecting the body from external antigens. The Arctic fox is an important member of furbearer farming, but due to the lack of research on the immune system of the Arctic fox, animal welfare regarding Arctic fox farming has still not received enough attention. In this study, we used the Arctic fox as a research subject, described the gene locus structure of the Arctic fox immunoglobulin germline by genome comparison, and analysed the mechanism of expression diversity of the antibody pool of the Arctic fox by rapid amplification of cDNA 5' ends and high-throughput sequencing.
View Article and Find Full Text PDFBlood Cancer J
December 2024
Center for Multiple Myeloma, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA.
Multiple myeloma (MM) remains incurable despite novel therapeutics. A major contributor to the development of relapsed/refractory and resistant MM is extraosseous extramedullary disease (EMD), whose molecular biology is still not fully understood. We analyzed 528 MM patients who presented to our institution between 2014 and 2021 and who had undergone molecular testing.
View Article and Find Full Text PDFNeural Regen Res
November 2025
School of Life Sciences, South China Normal University, Guangzhou, Guangdong Province, China.
JOURNAL/nrgr/04.03/01300535-202511000-00029/figure1/v/2024-12-20T164640Z/r/image-tiff Neuronal activity, synaptic transmission, and molecular changes in the basolateral amygdala play critical roles in fear memory. Cylindromatosis (CYLD) is a deubiquitinase that negatively regulates the nuclear factor kappa-B pathway.
View Article and Find Full Text PDFNucleic Acids Res
December 2024
Junior Research Group RNA Biology of Fungal Infections, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (Leibniz-HKI), Beutenbergstraße 11A, 07745 Jena, Germany.
Increasing antifungal drug resistance is a major concern associated with human fungal pathogens like Aspergillus fumigatus. Genetic mutation and epimutation mechanisms clearly drive resistance, yet the epitranscriptome remains relatively untested. Here, deletion of the A.
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