16 research outputs found

    Ferric Chloride-Mediated Transacylation of <i>N</i>‑Acylsulfonamides

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    Transacylation of N-acylsulfonamides, which replaces the N-acyl group with a new one, is a challenging and underdeveloped fundamental transformation. Herein, a general method for transacylation of N-acylsulfonamides is presented. The transformation is enabled by coincident catalytic reactivities of FeCl3 for nonhydrolytic deacylation of N-acylsulfonamides and subsequent acylation of the resultant sulfonamides and can be conducted either stepwise or in a one-pot manner. GaCl3 and RuCl3·xH2O are similarly effective for the reaction. This method is mild, efficient, and operationally simple. A variety of functional groups such as halogeno, keto, nitro, cyano, ether, and ester are well tolerated, providing the transacylation products in good to excellent yields

    G‑Quadruplex Structures as a “Switch” Regulate ATF4 Expression in Ferroptotic HepG2 Cells

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    G-quadruplex (G4) is a noncanonical structure folded in a widespread manner by guanine-rich tandem repeated sequences. As a key response factor, activating transcription factor 4 (ATF4) has dual functions in managing iron-dependent ferroptosis by regulating amino acid synthesis and antioxidant-related gene expression. In our study, the activity of ATF4 expression was elevated in HepG2 cells induced by erastin. Based on preliminary bioinformatics analyses, the G-tract region, named WT, had high potential to form G4, and it was found that PDS could markedly weaken the increase of ATF4 expression by reducing the sensitivity of HepG2 cells toward erastin. In circular dichroism spectra, WT oligonucleotides showed characteristic molar ellipticity at specific wavelengths of parallel G4 structures, while corresponding single-base mutants possessed a weaker ability to form G4, which were consistent with immunostaining results. In addition, endogenous G4 formed by the WT motif was significantly destroyed in HepG2 cells treated with erastin. After being transfected with WT oligonucleotides, the levels of ATF4 mRNA decreased significantly regardless of being treated with erastin or not. Meanwhile, mutations of G-tracts could advantageously impact the luciferase expression downstream of an ATF4 promoter in reporter assays, manifesting that the decrease of endogenous G4 in the ATF4 promoter was positively associated with the expression enhanced by erastin in HepG2 cells

    Photo No.4 in CVM (Haze Degree: Slight, RH = 64.2%, PM<sub>2.5</sub> = 131.4μg/m<sup>3</sup>, PM<sub>10</sub> = 311.7μg/m<sup>3</sup>, Vis = 4.9 km, AQI = 431).

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    <p>Photo No.4 in CVM (Haze Degree: Slight, RH = 64.2%, PM<sub>2.5</sub> = 131.4μg/m<sup>3</sup>, PM<sub>10</sub> = 311.7μg/m<sup>3</sup>, Vis = 4.9 km, AQI = 431).</p

    Photo No.3 in CVM (Haze Degree: Light, RH = 70.4%, PM<sub>2.5</sub> = 139.6μg/m<sup>3</sup>, PM<sub>10</sub> = 291.5μg/m<sup>3</sup>, Vis = 3.2 km, AQI = 402).

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    <p>Photo No.3 in CVM (Haze Degree: Light, RH = 70.4%, PM<sub>2.5</sub> = 139.6μg/m<sup>3</sup>, PM<sub>10</sub> = 291.5μg/m<sup>3</sup>, Vis = 3.2 km, AQI = 402).</p
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