Publications by authors named "G Temaj"
Leukemia represents the most prevalent malignancy in children, constituting 30% of childhood cancer cases, with acute lymphoblastic leukemia (ALL) being particularly heterogeneous. This paper explores the role of alternative splicing in leukemia, highlighting its significance in cancer development and progression. Aberrant splicing is often driven by mutations in splicing-factor genes, which can lead to the production of variant proteins that contribute to oncogenesis.
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- Elastin is crucial for skin elasticity and decreases with age, making it a target for anti-aging products.
- RiboScreen technology was used to find ribosomal proteins that enhance the production of tropoelastin, identifying ribosomal protein L40 (eL40) as a key regulator.
- A small molecule that activates eL40 was discovered, leading to increased levels of tropoelastin in cells, suggesting potential applications in skincare and cardiovascular health.
The tumor suppressor proteins are key transcription factors involved in the regulation of various cellular processes, such as apoptosis, DNA repair, cell cycle, senescence, and metabolism. The tumor suppressor protein p53 responds to different type of stress signaling, such as hypoxia, DNA damage, nutrient deprivation, oncogene activation, by activating or repressing the expression of different genes that target processes mentioned earlier. p53 has the ability to modulate the activity of many other proteins and signaling pathway through protein-protein interaction, post-translational modifications, or non-coding RNAs.
View Article and Find Full Text PDFIt is known that more than 10 % of genetic diseases are caused by a mutation in protein-coding mRNA (premature termination codon; PTC). mRNAs with an early stop codon are degraded by the cellular surveillance process known as nonsense-mediated mRNA decay (NMD), which prevents the synthesis of C-terminally truncated proteins. Up-frameshift-1 (UPF1) has been reported to be involved in the downregulation of various cancers, and low expression of UPF1 was shown to correlate with poor prognosis.
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- Severe junctional epidermolysis bullosa is a rare genetic skin disease mostly caused by harmful mutations in the LAMB3 gene, which is essential for skin structure.
- Current treatments using translational readthrough-inducing drugs are limited by toxicity, while ribosome editing offers a more targeted approach.
- This study found that repurposing the drugs artesunate and atazanavir, alongside ribosomal protein L35, significantly increases the production of the full-length LAMB3 protein in affected cells, suggesting a promising therapeutic option for the disease.