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In plasma, the zymogens factor XII (FXII) and prekallikrein reciprocally convert each other to the proteases FXIIa and plasma kallikrein (PKa). PKa cleaves high-molecular-weight kininogen (HK) to release bradykinin, which contributes to regulation of blood vessel tone and permeability. Plasma FXII is normally in a "closed" conformation that limits activation by PKa.

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The enduring pathogenicity of can be attributed to its lipid-rich cell wall, with mycolic acids (MAs) being a significant constituent. Different MAs' fluidity and structural adaptability within the bacterial cell envelope significantly influence their physicochemical properties, operational capabilities, and pathogenic potential. Therefore, an accurate conformational representation of various MAs in aqueous media can provide insights into their potential role within the intricate structure of the bacterial cell wall.

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enterotoxin-claudin pore complex: Models for structure, mechanism of pore assembly and cation permeability.

Comput Struct Biotechnol J

December 2024

Clinical Physiology/Nutritional Medicine, Department of Gastroenterology, Rheumatology and Infectious Diseases, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Hindenburgdamm 30, 12203 Berlin, Germany.

The pore-forming enterotoxin (CPE), a common cause of foodborne diseases, facilitates Ca influx in enterocytes, leading to cell damage. Upon binding to certain claudins (e.g.

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Inhibition of hydrogen peroxide-induced senescence markers by yeast-derived vacuoles in human lung fibroblasts.

Biochim Biophys Acta Mol Cell Res

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Graduate School of Semiconductor and Chemical Engineering, Jeonbuk National University, 567 Baekje-daero, Deokjin-Gu, Jeonju, Jeonbuk 54896, South Korea. Electronic address:

Senescence significantly contributes to aging in various tissues, influenced by factors such as lysosomal alkalinization, which disrupts autophagic flux and accumulates toxic substances. This disruption leads to oxidative stress, increased lysosomal permeability, cellular senescence, and apoptosis. Similar to mammalian lysosomes, S.

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Objectives: Exploring the role of VDAC1 in hepatocyte apoptosis during acute liver injury induced by obstructive jaundice.

Materials And Methods: Animal and cell models were established to investigate possible mechanisms during acute liver injury induced by OJ. Blood was collected for liver function assessment.

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