Rapid Analysis of Trace Nickel in Hydrogenated Cottonseed Oil by Microwave Digestion Prior to Its Inductively Coupled Plasma Mass Spectrometry Determination
SPECTROSCOPY LETTERS
Authors: Meng, Zuchao; Zhang, Ni
Abstract
A microwave-assisted digestion procedure for the analysis of trace nickel in hydrogenated cottonseed oil prior to its determination by inductively coupled plasma mass spectrometry was constructed for the first time. The proposed microwave-assisted digestion avoided tarnishing of sample in the process of sample pretreatment and reduced the cycle of analysis. The programs of microwave digestion and the parameters of inductively coupled plasma mass spectrometry were optimized. The accuracy of the proposed method was investigated by analyzing real samples. The results were compared with the ones by pressurized-PTFE-bomb acid digestion and ones by United States Pharmacopeia 28 (USP28) method. This method served as a relatively quick matrix destruction technique compared with other present methods for the quantization of metals in oil.
53BP1 and USP28 mediate p53 activation and G1 arrest after centrosome loss or extended mitotic duration
JOURNAL OF CELL BIOLOGY
Authors: Meitinger, Franz; Anzola, John V.; Kaulich, Manuel; Richardson, Amelia; Stender, Joshua D.; Benner, Christopher; Glass, Christopher K.; Dowdy, Steven F.; Desai, Arshad; Shiau, Andrew K.; Oegema, Karen
Abstract
In normal human cells, centrosome loss induced by centrinone-a specific centrosome duplication inhibitor-leads to irreversible, p53-dependent G1 arrest by an unknown mechanism. A genome-wide CRI SPR/Cas9 screen for centrinone resistance identified genes encoding the p53-binding protein 53BP1, the deubiquitinase USP28, and the ubiquitin ligase TRIM37. Deletion of TP53BP1, USP28, or TRIM37 prevented p53 elevation in response to centrosome loss but did not affect cytokinesis failure-induced arrest or p53 elevation after doxorubicin-induced DNA damage. Deletion of TP53BP1 and USP28, but not TRIM37, prevented growth arrest in response to prolonged mitotic duration. TRIM37 knockout cells formed ectopic centrosomal-component foci that suppressed mitotic defects associated with centrosome loss. TP53BP1 and USP28 knockouts exhibited compromised proliferation after centrosome removal, suggesting that centrosome-independent proliferation is not conferred solely by the inability to sense centrosome loss. Thus, analysis of centrinone resistance identified a 53BP1-USP28 module as critical for communicating mitotic challenges to the p53 circuit and TRIM37 as an enforcer of the singularity of centrosome assembly.