Publications by authors named "Larisa Okorokova"

Tyrosyl-DNA phosphodiesterase 1 (TDP1) is a human DNA repair protein. It is a member of the phospholipase D family based on structural similarity. TDP1 is a key enzyme of the repair of stalled topoisomerase 1 (TOP1)-DNA complexes.

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  • - This study explores how repetitive DNA sequences influence the social structures of honeybees, focusing on two subspecies and their genomic differences.
  • - While much is known about the Notch signaling pathway in caste formation, the specific elements that regulate gene expression (cis-regulatory sequences) are still not fully identified.
  • - The research highlights a unique chromatin state linked to these repetitive elements, suggesting they might play a role in developing new regulatory functions, even though their impact on gene expression during caste differentiation was minimal.
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Introduction: Culturing of human neural stem cells (NSCs) derived from induced pluripotent stem cells (iPSC) is a promising area of research, as these cells have the potential to treat a wide range of neurological, neurodegenerative and psychiatric diseases. However, the development of optimal protocols for the production and long-term culturing of NSCs remains a challenge. One of the most important aspects of this problem is to determine the stability of NSCs during long-term in vitro passaging.

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  • Topoisomerase 1 (TOP1) is crucial for DNA functions like replication and is targeted by anticancer drugs such as topotecan, which can cause cell death by stabilizing the TOP1 cleavage complex.
  • Tyrosyl-DNA phosphodiesterase 1 (TDP1) can remove this complex, thereby reducing the effectiveness of topotecan.
  • A study comparing wild type and PARP1 knockout HEK293A cells revealed that PARP1 deficiency led to significantly more changes in gene expression when treated with topotecan and a TDP1 inhibitor, affecting pathways related to cancer development and DNA repair.
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Repetitive elements (REs) occupy a significant part of eukaryotic genomes and are shown to play diverse roles in genome regulation. During embryogenesis of the sea urchin, a large number of REs are expressed, but the role of these elements in the regulation of biological processes remains unknown. The aim of this study was to identify the RE expression at different stages of embryogenesis.

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The ability of exogenous low ouabain concentrations to affect claudin expression and therefore epithelial barrier properties was demonstrated previously in cultured cell studies. We hypothesized that chronic elevation of circulating ouabain in vivo can affect the expression of claudins and tight junction permeability in different tissues. We tested this hypothesis in rats intraperitoneally injected with ouabain (1 μg/kg) for 4 days.

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Cholera toxin is commonly known to induce chloride secretion of the intestine. In recent years, effects on epithelial barrier function have been reported, indicating synergistic co-regulation of transporters and tight junction proteins. Our current study focused on the analysis of cholera toxin effects on transepithelial resistance and on tight junction proteins, the latter known as structural correlates of barrier function.

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Objective: The morphology and functions of the proximal and distal large intestine are not the same. The incidence of colorectal cancer in these regions is also different, as tumors more often appear in the descending colon than in the ascending colon. Inflammatory bowel disease and colorectal cancer can increase transepithelial permeability, which is a sign of reduced intestinal barrier function.

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  • High doses of epidermal growth factor (EGF) can paradoxically trigger cell death (apoptosis) in A431 epidermoid carcinoma cells that overexpress EGF receptors, despite EGF being known to promote cell growth.
  • The study reveals that the activation of the STAT1 transcription factor is vital for EGF-induced apoptosis in these cells.
  • Researchers found that the p38 MAP kinase pathway is crucial in this process, as inhibiting it reduced both the growth-inhibiting and pro-apoptotic effects of EGF by decreasing the phosphorylation of STAT1, specifically on tyrosine 701.
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