, 2009). Thus, the question of arsenite binding is of great interest to synthetic biologists involved in engineering of novel molecular entities that could be used in arsenite detection and decontamination. Most of the molecular models of arsenite binding involve thiol-based chemistry. In fact, most of the proteins that have been identified to bind to arsenite and thus have been inactivated by it do so through Cys residues (Hughes,

2002; Kitchin & Wallace, 2004). However, neither Cys residue nor Tyr residues, which have also been reported to bind arsenite in some proteins (Page & Wilson, 1985), are present within the sensory domain of AroS. Perhaps the difference in the mode of binding arsenite is not too surprising when considering the function that AroS performs. This protein needs to be able to bind arsenite reversibly and to Palbociclib concentration be able to respond to changes in arsenite concentrations. Presently, we cannot provide Venetoclax a definitive answer of what the mechanism of arsenite sensing is; however, our work provides a foundation for further structural and mechanistic analysis of this regulatory system. In addition, not only do arsenite-oxidizing

bacteria need to be able to sense the presence of arsenite in the environment, but they also need means of evading arsenite toxicity. Our studies have demonstrated for the first time that a mutation in aroS has an effect on the growth of NT-26 in the presence of arsenite. Thus, AroS may play an additional role in the regulation of a pathway involved in tolerance to arsenite. T.H.O. is supported by a Natural Environment Research Council studentship (14404A). Fig. S1. 1D 1H NMR spectra for AroS226–490H273N protein that lacks autophosphorylation activity. Please note: Wiley-Blackwell is not responsible for

the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“In this issue, Tordato et al. [1] present interesting findings from the Italian Cohort of Antiretrovial Naive patients (ICONA) study group considering the estimated glomerular 3-mercaptopyruvate sulfurtransferase filtration rate (eGFR) and risk factors for mild renal dysfunction, defined as eGFR<90 mL/min/1.73 m2. Since the introduction of combination antiretroviral therapy and subsequent dramatic improvements in morbidity and mortality [2], patients with HIV infection live longer and research has increasingly been carried out on comorbidities, including renal disease [3]. There have been a number of recent studies focusing on renal function using different definitions and methodologies which can lead to conflicting results and difficulty in interpreting data. GFR is commonly estimated using the Cockcroft–Gault (CG) formula [4], the Modified Diet in Renal Disease (MDRD) equations [5], and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation [6].