Background Maternal executive function and household regulation both are critical aspects of optimal childrearing, but their interplay is not understood. We tested the hypotheses that 1) the link between challenging child conduct problems and harsh parenting would be strongest for mothers with poorer executive function and weakest among those with better executive function, and 2) this mechanism would be further moderated by the degree of household chaos. Methods The socioeconomically diverse sample included 147 mothers of 3-to-7 year old children. Mothers completed questionnaires and a laboratory assessment of executive function. Results Consistent with hypotheses, harsh parenting was linked with child conduct problems only among mothers with poorer executive function. This effect was particularly strong in calm, predictable environments, but was not evident in chaotic environments. Conclusion Maternal executive function is critical to minimizing harsh parenting in the context of challenging child behavior, but this self-regulation process may not operate well in chaotic environments.

Ferroptosis is a regulated form of necrotic cell death implicated in carcinogenesis and neurodegeneration that is driven by phospholipid peroxidation. Lipid-derived electrophiles (LDEs) generated during this process can covalently modify proteins ("carbonylation") and affect their functions. Here we report the development of a quantitative chemoproteomic method to profile carbonylations in ferroptosis by an aniline-derived probe. Using the method, we established a global portrait of protein carbonylations in ferroptosis with >400 endogenously modified proteins and for the first time, identified >20 residue sites with endogenous LDE modifications in ferroptotic cells. Specifically, we discovered and validated a novel cysteine site of modification on voltage-dependent anion-selective channel protein 2 (VDAC2) that might play an important role in sensitizing LDE signals and mediating ferroptosis. Our results will contribute to the understanding of ferroptotic signaling and pathogenesis and provide potential biomarkers for ferroptosis detection.

Despite numerous studies on ebselen over the past decade, its cellular targets remain obscure. Here we synthesized a biotinylated ebselen probe (biotin-ebselen) and characterized ebselen-binding proteins via an efficient activity-based protein profiling (ABPP) method, which allowed for the robust identification of 462 targeted proteins in HeLa cells. This first work of global target profiling of ebselen will be helpful to re-design ebselen-based therapy appropriately in clinical trials.

Inspired by native chemical ligation, we apply thioester probes to profile protein N-homocysteinylation with chemical proteomics strategy.

What happens to everyday social interactions when other‐race recognition fails? Here, we provide the first formal investigation of this question. We gave East Asian international students (N = 89) a questionnaire concerning their experiences of the other‐race effect (ORE) in Australia, and a laboratory test of their objective other‐race face recognition deficit using the Cambridge Face Memory Test (CFMT). As a ‘perpetrator’ of the ORE, participants reported that their problems telling apart Caucasian people contributed significantly to difficulties socializing with them. Moreover, the severity of this problem correlated with their ORE on the CFMT. As a ‘victim’ of the ORE, participants reported that Caucasians' problems telling them apart also contributed to difficulties socializing. Further, 81% of participants had been confused with other Asians by a Caucasian authority figure (e.g., university tutor, workplace boss), resulting in varying levels of upset/difficulty. When compared to previously established contributors to international students' high rates of social isolation, ORE‐related problems were perceived as equally important as the language barrier and only moderately less important than cultural differences. We conclude that the real‐world impact of the ORE extends beyond previously identified specialized settings (eyewitness testimony, security), to common everyday situations experienced by all humans.

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Protein 4′‐phosphopantetheinylation is an essential post‐translational modification (PTM) in prokaryotes and eukaryotes. So far, only five protein substrates of this specific PTM have been discovered in mammalian cells. These proteins are known to perform important functions, including fatty acid biosynthesis and folate metabolism, as well as β‐alanine activation. To explore existing and new substrates of 4′‐phosphopantetheinylation in mammalian proteomes, we designed and synthesized a series of new pantetheine analogue probes, enabling effective metabolic labelling of 4′‐phosphopantetheinylated proteins in HepG2 cells. In combination with a quantitative chemical proteomic platform, we enriched and identified all the currently known 4′‐phosphopantetheinylated proteins with high confidence, and unambiguously determined their exact sites of modification. More encouragingly, we discovered, using targeted chemical proteomics, a potential 4′‐phosphopantetheinylation site in the protein of mitochondrial dehydrogenase/reductase SDR family member 2 (DHRS2).