Fe−N−C single-atom catalysts (SACs) exhibit high activity for oxygen reduction reaction (ORR). However, it remains controversial how the active center mediates catalysis, and the predicted potential deviates from experimental results, hindering development of ideal SACs. Here, using first-principles calculations, we present a microkinetic model for ORR on Fe−N−C SACs, disclosing a self-adjusting mechanism induced by its intrinsic intermediate. The modeling results show that the single-atom Fe site of the FeN 4 center of Fe−N−C is covered with an intermediate OH* from 0.28 to 1.00 V. Remarkably, such OH* becomes part of the active moiety, Fe(OH)N 4 , and can optimize intermediate bindings on the Fe site, exhibiting a theoretical half-wave potential of ∼0.88 V. Partial current density analysis reveals the dominating associative path over the dissociative ones. In addition, ORR on Mn−N−C and Co−N−C SACs is unveiled. This work demonstrates the necessity of assessing the effect of intrinsic intermediates in singleatom catalysis and provides practical guidance for rational design of high-performance SACs.

Facile design of low‐cost and highly active catalysts from earth‐abundant elements is favorable for the industrial application of water splitting. Here, a simple strategy to synthesize an ultrathin molybdenum disulfide/nitrogen‐doped reduced graphene oxide (MoS2/N‐RGO‐180) nanocomposite with the enlarged interlayer spacing of 9.5 Å by a one‐step hydrothermal method is reported. The synergistic effects between the layered MoS2 nanosheets and N‐doped RGO films contribute to the high activity for hydrogen evolution reaction (HER). MoS2/N‐RGO‐180 exhibits the excellent catalytic activity with a low onset potential of −5 mV versus reversible hydrogen elelctrode (RHE), a small Tafel slope of 41.3 mV dec−1, a high exchange current density of 7.4 × 10−4 A cm−2, and good stability over 5 000 cycles under acidic conditions. The HER performance of MoS2/N‐RGO‐180 nanocomposite is superior to the most reported MoS2‐based catalysts, especially its onset potential and exchange current density. In this work, a novel and simple method to the preparation of low‐cost MoS2‐based electrocatalysts with the extraordinary HER performance is presented.

Tumor necrosis factor receptor-associated factor 6 (TRAF6) is critical for mediating Toll-like receptor (TLR)-interleukin 1 receptor (IL-1R) signaling and subsequent activation of NF-kappaB and AP-1, transcriptional activators of innate immunity. Here we show that beta-arrestins, a family of multifunctional proteins, directly interacted with TRAF6 after TLR-IL-1R activation. Formation of the beta-arrestin-TRAF6 complex prevented autoubiquitination of TRAF6 and activation of NF-kappaB and AP-1. Endotoxin-treated beta-arrestin 2-deficient mice had higher expression of proinflammatory cytokines and were more susceptible to endotoxic shock. Thus, beta-arrestins are essential negative regulators of innate immune activation via TLR-IL-1R signaling.