Publications by authors named "Amalia Goula"
Ionising radiation (IR) is widely used in cancer treatment, including for head and neck squamous cell carcinoma (HNSCC), where it induces significant DNA damage leading ultimately to tumour cell death. Among these lesions, DNA double strand breaks (DSBs) are the most threatening lesion to cell survival. The two main repair mechanisms that detect and repair DSBs are non-homologous end joining (NHEJ) and homologous recombination (HR).
View Article and Find Full Text PDFWDR5 is a broadly studied, highly conserved key protein involved in a wide array of biological functions. Among these functions, WDR5 is a part of several protein complexes that affect gene regulation via post-translational modification of histones. We collected data from 11 unrelated individuals with six different rare germline missense variants in ; one identical variant was found in five individuals and another variant in two individuals.
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- The 53BP1-RIF1-shieldin pathway is crucial for maintaining genome stability by preventing the degradation of DNA ends at double-strand breaks (DSBs).
- RIF1 is recruited to DSBs through interaction with phospho-53BP1 and is influenced by the methylation of histone H3 at lysine 4, mediated by SETD1A-BOD1L.
- Impairing SETD1A or BOD1L disrupts RIF1's ability to localize to DSBs, leading to issues in DNA repair and potential therapeutic resistance in certain cancer cells, highlighting the pathway's clinical significance.
Article Synopsis
- Methylation of lysine 4 on histone H3 (H3K4) by the enzyme SETD1A is crucial for maintaining genome stability by safeguarding newly-replicated DNA from degradation.
- This process involves the regulation of nucleosome movement, which is aided by FANCD2, a key player in preserving genome integrity.
- The findings highlight the importance of SETD1A in influencing chemo-sensitivity, suggesting its role may be critical in cancer treatment response.
Article Synopsis
- Components of the Fanconi anemia and homologous recombination pathways are essential for protecting newly replicated DNA from degradation, thus maintaining genome stability.
- The lysine methyltransferase SETD1A plays a key role in preventing damage to stalled replication forks by catalyzing the methylation of histone H3 at Lys4 (H3K4), which enhances the function of FANCD2 as a histone chaperone.
- Depleting SETD1A or inhibiting H3K4 methylation leads to the degradation of replication forks, highlighting how epigenetic modifications and histone mobility are critical for genome stability by controlling nucleolytic activity.
A new biocatalyst was prepared by immobilization of Saccharomyces cerevisiae AXAZ-1 yeast cells in the matrix of corn starch gel. This biocatalyst was used for repeated batch fermentations of glucose and grape must at various sugar concentrations (110-280 g/L) and low-temperature winemaking (5 degrees C). The biocatalyst retained its operational stability for a long period, and it was proved to be capable of producing dry and semisweet wines.
View Article and Find Full Text PDFBackground: A study was conducted at the University Hospital of Patras between January 2002 and December 2003 to investigate antibiotic resistance patterns and clonality of Salmonella enterica in southwestern Greece.
Methods: Ninety-five isolates recovered from different outpatients were characterized by specific antisera and were tested for their susceptibility to various antimicrobial agents. Clones were identified by pulsed-field gel electrophoresis (PFGE) of XbaI chromosomal DNA digests.