Publications by authors named "Monika Gelazauskaite"
Article Synopsis
- Pancreatic adenocarcinoma (PA) has a very low 5-year survival rate of less than 5%, and existing treatments are minimally effective, with WNT/β-catenin signaling identified as a key pathway often mutated in PA.
- Researchers created human PA cell lines lacking β-catenin through targeted genetic modification and found that these cells maintained normal growth and survival without significant changes in their overall morphology.
- Although the absence of β-catenin was noted, there were downregulations in proteins related to cell adhesion, while plakoglobin levels increased; targeting plakoglobin led to impaired cell contacts and altered E-cadherin localization, indicating plakoglobin's role in maintaining cell adhesion in the absence of β-catenin
Background: Formation of site specific genomic double strand breaks (DSBs), induced by the expression of a pair of engineered zinc-finger nucleases (ZFNs), dramatically increases the rates of homologous recombination (HR) between a specific genomic target and a donor plasmid. However, for the safe use of ZFN induced HR in practical applications, possible adverse effects of the technology such as cytotoxicity and genotoxicity need to be well understood. In this work, off-target activity of a pair of ZFNs has been examined by measuring the ratio between HR and illegitimate genomic integration in cells that are growing exponentially, and in cells that have been arrested in the G2/M phase.
View Article and Find Full Text PDFSingle-stranded oligonucleotides (ssODNs) and zinc-finger nucleases (ZFNs) are two approaches that are being pursued to achieve sequence specific genome modification. ZFNs induce high rates of homologous recombination (HR) between the target sequence and a given donor by introducing site-specific genomic double-strand breaks (DSBs). The mode of action that is used by ssODNs remains largely unknown, but may involve genomic integration of the ssODNs.
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