Publications by authors named "D Kucerova"

We tested the effects of galactoglucomannan oligosaccharides (GGMOs) and/or cadmium (Cd) on peroxidase activity and the proteome in maize (Zea mays L.) roots and leaves. Our previous work confirmed that GGMOs ameliorate the symptoms of Cd stress in seedlings.

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Article Synopsis
  • Retroviruses integrate into host genomes to create proviruses for stable viral gene expression, but their transcription can be hindered by epigenetic silencing.
  • Gammaretroviruses (γRVs) tend to integrate into active promoter and enhancer regions, leading to higher transcriptional activity due to their preferential integration preference.
  • The study shows that while some γRV long terminal repeats (LTRs) are quickly silenced, others can sustain long-term expression even in less favorable chromatin environments, with alternative retroviruses like feline leukemia virus and koala retrovirus also contributing to stable, varied gene expression.
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Syncytin-1, a human fusogenic protein of retroviral origin, is crucial for placental syncytiotrophoblast formation. To mediate cell-to-cell fusion, Syncytin-1 requires specific interaction with its cognate receptor. Two trimeric transmembrane proteins, Alanine, Serine, Cysteine Transporters 1 and 2 (ASCT1 and ASCT2), were suggested and widely accepted as Syncytin-1 cellular receptors.

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Genetic editing of the germline using CRISPR/Cas9 technology has made it possible to alter livestock traits, including the creation of resistance to viral diseases. However, virus adaptability could present a major obstacle in this effort. Recently, chickens resistant to avian leukosis virus subgroup J (ALV-J) were developed by deleting a single amino acid, W38, within the ALV-J receptor NHE1 using CRISPR/Cas9 genome editing.

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Desmoglein-2 mutations are detected in 5-10% of patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Endurance training accelerates the development of the ARVC phenotype, leading to earlier arrhythmic events. Homozygous mutant mice develop a severe ARVC-like phenotype.

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