3 research outputs found
State of ions copper(II) and cobalt(II) in phase carboxyl cation resin according to the methods ESDR and EPR
The properties of the Tokheim-250 carboxylic cation exchange resin and its selectivity to Co2 + and Ni2+ ions are studied. The values of the sorption capacity for the Co2+ and Ni2+ ions, the effective ionization constant of the functional groups (pKa = 6,59), and the values of the ion distribution coefficients (~ 103) are calculated. Founded that the selectivity of the sorption of Co2+ increased to Ni2 +. In this regard, carboxylic cation exchanger Tokem-250 samples with nickel ion was used to create spherical catalysts. The developed spherical materials have catalytic activity in the reactions of deep and partial oxidation of n-heptane
Restriction factor screening identifies RABGAP1L-mediated disruption of endocytosis as a host antiviral defense
Host interferons (IFNs) powerfully restrict viruses through the action of several hundred IFN-stimulated gene (ISG) products, many of which remain uncharacterized. Here, using RNAi screening, we identify several ISG restriction factors with previously undescribed contributions to IFN-mediated defense. Notably, RABGAP1L, a Tre2/Bub2/Cdc16 (TBC)-domain-containing protein involved in regulation of small membrane-bound GTPases, robustly potentiates IFN action against influenza A viruses (IAVs). Functional studies reveal that the catalytically active TBC domain of RABGAP1L promotes antiviral activity, and the RABGAP1L proximal interactome uncovered its association with proteins involved in endosomal sorting, maturation, and trafficking. In this regard, RABGAP1L overexpression is sufficient to disrupt endosomal function during IAV infection and restricts an early post-attachment, but pre-fusion, stage of IAV cell entry. Other RNA viruses that enter cells primarily via endocytosis are also impaired by RABGAP1L, while entry promiscuous SARS-CoV-2 is resistant. Our data highlight virus endocytosis as a key target for host defenses.ISSN:2666-3864ISSN:2211-124