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Apoptosis: Cellular Signaling and Molecular Mechanisms
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Rosemary B. Evans, John A. Cidlowski
A Ca2+/Mg2+-dependent nuclease has been isolated from S49.1 rat thymoma cells and from rat thymocyte nuclei from adrenalectomized rats treated with glucocorticoids.20,21 Induction of this activity is inhibited by the glucocorticoid antagonist RU 486, indicating the response is glucocorticoid receptor mediated.20 Glucocorticoid treatment causes a Ca2+ influx in these cells. If this Ca2+ flux is inhibited by intracellular buffering by quin-2 or incubation in Ca2+-free medium, cell death will not occur, demonstrating that this intracellular increase in Ca2+ is required for apoptosis in these cells.2 This nuclease is 18 kDa when resolved by SDS-PAGE and is, therefore, referred to as NUC 18; however, its molecular mass when resolved by size exclusion chromatography is approximately 25 kDa.21,22 It displays an optimal nuclease activity at a pH of 7.0 to 8.5 and is inhibited by Zn2+, Na+, and the nuclease inhibitor aurintricarboxylic acid (ATCA).22 Nuclease activity is increased approximately twofold when Mg2+ or Mn2+ is present in combination with Ca2+.
Replicase
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
The initiation of the Qβ replicase-directed synthesis, but not elongation of the initiated polynucleotide chains, was inhibited also by low concentrations of the aurintricarboxylic acid (ATA) dye (Blumenthal and Landers 1973).
Radionuclide Generators
Published in Garimella V. S. Rayudu, Lelio G. Colombetti, Radiotracers for Medical Applications, 2019
Aluminum ions in the eluates can be detected by the formation of a pink “lake” with a solution of aluminon (trisodium salt of aurintricarboxylic acid) in 3 M ammonium acetate. The intensity of the color, as compared to the colors produced by standard solutions of aluminum, will indicate the concentration of aluminum ions in the eluates. It is believed that concentration larger than 10 μg/mℓ could interfere with the quality of technetium labeling.
Aurintricarboxylic acid mitigates cigarette smoke extract induced oxidative stress and pulmonary inflammation via inhibition of NF-ҡB/p65 signaling
Published in Toxicology Mechanisms and Methods, 2023
Kusum Devi, Yatendra Singh, Sanjeev Kanojiya, Baisakhi Moharana
Aurintricarboxylic acid (ATA) is trisodium salt and a member of quinomethanes. Chemically, ATA is a polyanionic aromatic compound especially known for its protein and nucleic acid interaction and protein synthesis inhibition properties (Stewart et al. 1971; Blumenthal and Landers 1973). More importantly, ATA has been recognized for its potent and selective inhibition of enzymatic replication of various viruses, including SARS coronavirus (SARS CoV) (He R et al. 2004), Zika (Park et al. 2019), Influenza (Hashem et al. 2009), and Vaccinia (Myskiw et al. 2007) and inhibits apoptosis and regulates cell proliferation in myeloid cells (Andrew et al. 1999). Currently, ATA is identified as a selective inhibitor of the TWEAK/Fn14 signaling pathway (Roos et al. 2017). It is also known for its antagonistic effect on LPS/IFN-γ-induced inflammation (Laufenberg et al. 2014). However, there is no study available to demonstrate the anti-oxidative and anti-inflammatory role of ATA in cigarette smoke-induced pulmonary inflammation. Therefore, we aimed to decipher the role of ATA on cigarette smoke extract-induced pulmonary inflammation in in vivo and in vitro models.
Understanding host responses to equine encephalitis virus infection: implications for therapeutic development
Published in Expert Review of Anti-infective Therapy, 2022
Kylene Kehn-Hall, Steven B. Bradfute
Acriflavine suppressed VEEV TC-83, VEEV TrD, EEEV, WEEV, WNV, but not VSV replication. Acriflavine is typically used as an antiseptic, but more recently was shown to inhibit Ago2, a protein involved in miRNA processing [144]. The importance of Ago2 for alphavirus replication was further shown through MEFs lacking Ago2 having decreased VEEV TC-83 viral RNA levels, structural protein production, and infectious titers [141]. In addition, multiple inhibitors of the miRNA machinery, including aurintricarboxylic acid (ATA), oxidopamine hydrochloride (OXD) and suramin (SUR), acriflavine, and poly L lysine, suppressed VEEV TC-83 replication, with acriflavine being the most potent. Acriflavine partially protected C3H/HeN mice from VEEV TC-83 infection, but did not have a protective effect on BALB/c mice infected with VEEV TrD, indicating that inhibition of Ago2 alone is not sufficient to protect mice from a fully virulent VEEV infection.