Escherichia colidam cells have an active but non-directed mismatch repair system; therefore, assembly of MutSLH complex at a mismatched base pair can result in MutH-mediated cleavage of GATC sites in both DNA strands. Unpaired double-strand breaks on a fraction of the replication errors occurring in dam cells presumably cause cell death, selectively eliminating these putative mutants from the population. We show that E. colidam cells transformed with plasmids containing either the mutS, mutL or mutH gene display a mutation frequency three to eight times lower than that of the parental dam strain, due to increased mismatch-stimulated cell killing. Transformed strains are also more susceptible to killing by the base analogue 2-aminopurine. However, dam and dam transformed cells have similar duplication time, proportion of live/dead cells and morphology.
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http://dx.doi.org/10.1016/j.mrfmmm.2007.07.006 | DOI Listing |
J Hematol Oncol
January 2025
Center for Cell Therapy & Regenerative Medicine (CCRG), Antwerp University Hospital (UZA), Edegem, Belgium.
Cell therapies, including tumor antigen-loaded dendritic cells used as therapeutic cancer vaccines, offer treatment options for patients with malignancies. We evaluated the feasibility, safety, immunogenicity, and clinical activity of adjuvant vaccination with Wilms' tumor protein (WT1) mRNA-electroporated autologous dendritic cells (WT1-mRNA/DC) in a single-arm phase I/II clinical study of patients with advanced solid tumors receiving standard therapy. Disease status and immune reactivity were evaluated after 8 weeks and 6 months.
View Article and Find Full Text PDFMol Neurodegener
January 2025
Department of Neurobiology and Behavior, Charlie Dunlop School of Biological Sciences, University of California, Irvine, CA, 92697-4545, USA.
Background: Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer's Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Myelin loss induces neural dysfunction and contributes to the pathophysiology of neurodegenerative diseases, injury conditions, and aging. Because remyelination is often incomplete, better understanding endogenous remyelination and developing remyelination therapies that restore neural function are clinical imperatives. Here, we use in vivo two-photon microscopy and electrophysiology to study the dynamics of endogenous and therapeutic-induced cortical remyelination and functional recovery after cuprizone-mediated demyelination in mice.
View Article and Find Full Text PDFTissue Cell
January 2025
Urology Research Center, Tehran University of Medical Sciences, Tehran, Iran. Electronic address:
Objective: Research and tools are necessary for understanding prostate cancer biology. 3D cell culture models have been created to overcome the limitations of animal models and 2D cell culture. The amniotic membrane (AM), a natural biomaterial, emerges as an ideal scaffold for 3D cultures due to its accessibility and incorporation of the extracellular matrix (ECM) in both solid and liquid forms.
View Article and Find Full Text PDFbioRxiv
December 2024
Division of Developmental Biology, Eunice Kennedy-Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD 20892, USA.
The eukaryotic genome is packaged into chromatin, which is composed of a nucleosomal filament that coils up to form more compact structures. Chromatin exists in two main forms: euchromatin, which is relatively decondensed and enriched in transcriptionally active genes, and heterochromatin, which is condensed and transcriptionally repressed . It is widely accepted that chromatin architecture modulates DNA accessibility, restricting the access of sequence-specific, gene-regulatory, transcription factors to the genome.
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