Publications by authors named "Seonha Park"

Article Synopsis
  • Atopic dermatitis (AD) involves a Th2 inflammatory response damaging the skin, and there's a strong link between this condition and a specific strain of bacteria, A2-165, known for producing butyrate.
  • Researchers have determined the 3D structure of an important enzyme, 3-hydroxybutyryl-CoA dehydrogenase (A2HBD), using advanced X-ray techniques, revealing its interactions with key molecules like acetoacetyl-CoA and NAD.
  • The study highlights significant conformational changes in A2HBD when substrates bind, particularly noting how specific residues contribute to substrate recognition and the enzyme's overall catalytic activity.
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The exosome multiprotein complex plays a critical role in RNA processing and degradation. This system governs the regulation of mRNA quality, degradation in the cytoplasm, the processing of short noncoding RNA, and the breakdown of RNA fragments. We determined two crystal structures of exosome components from (): one with a resolution of 2.

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Prolyl-tRNA synthetase 1 (PARS1) has attracted much interest in controlling pathologic accumulation of collagen containing high amounts of proline in fibrotic diseases. However, there are concerns about its catalytic inhibition for potential adverse effects on global protein synthesis. We developed a novel compound, DWN12088, whose safety was validated by clinical phase 1 studies, and therapeutic efficacy was shown in idiopathic pulmonary fibrosis model.

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Cytochrome P450 BM3 (CYP102A1) from Bacillus megaterium is a self-sufficient monooxygenase that consists of a heme domain and FAD/FMN-containing reductase domain (BMR). In this report, the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and 5-cyano-2,3-ditolyl tetrazolium chloride (CTC) by BMR was evaluated as a method for monitoring BMR activity. The electron transfer proceeds from NADPH to BMR and then to BMR substrates, MTT and CTC.

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The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer's disease (AD). Evidence suggests that the effect of apoE isoforms on amyloid-β (Aβ) accumulation in the brain plays a critical role in AD pathogenesis. Like in humans, apoE4 expression in animal models that develop Aβ amyloidosis results in greater Aβ and amyloid deposition than with apoE3 expression.

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