RESUMO
The poor kinetic background with the four-electron transfer of the oxygen evolution reaction (OER) was eradicated using a nickel-based catalyst, which was identified as an alternative to noble-metal catalysts. Here, we report the simple in situ formation of an earth-abundant nickel oxyhydroxide (NiOOH) electrocatalyst for efficient OER in an alkaline medium. Electroless material preparation, namely, the direct modification of a gas diffusion layer (GDL) with a nickel salt, was studied, and the layered oxyhydroxide phase was found to influence the rate of the OER. Interestingly, complete OER studies were carried out without using any external binders; that is, the catalyst stabilized in an aqueous medium was directly exploited. The resulting in situ electrochemically tuned NiOOH@GDL shows a low overpotential of 294 mV to reach a current density of 20 mA cm-2, which is superior to most non-noble mono/bimetal oxides that have been studied as OER catalysts so far. The catalyst also shows better kinetics with a low Tafel slope value of 30 mV dec-1 for NiOOH@GDL-B. In addition, the stability of NiOOH@GDL-B was confirmed from a chronoamperometric study that was carried out for 30 h with no significant loss in activity. The electrochemical evolution of the materials was further scrutinized, and a high turnover frequency (TOF) of 1.1 × 10-4 s-1 was calculated at 300 mV. The consistency of the catalyst was proved with various post-OER characterization analyses, and it appears to be beneficial for developing an efficient electrocatalyst for OER in the near future.
RESUMO
The Yes-associated protein (YAP) is a downstream effector of the Hippo pathway and acts as a key transcription co-factor to regulate cell migration, proliferation, and survival. The Hippo pathway is evolutionarily conserved and controls tissue growth and organ size. Dysregulation and heterogeneity of this pathway are found in cancers, including oral squamous cell carcinoma (OSCC), leading to overexpression of YAP and its regulated proliferation machinery. The activity of YAP is associated with its nuclear expression and is negatively regulated by the Hippo kinase-mediated phosphorylation resulting in an induction of its cytoplasmic translocation. This review focuses on the role of YAP in OSCC in the context of cancer metastatic potential and highlights the latest findings about the heterogeneity of YAP expression and its nuclear transcription activity in oral cancer cell lines. The review also discusses the potential target of YAP in oral cancer therapy and the recent finding of the unprecedented role of the desmosomal cadherin desmoglein-3 (DSG3) in regulating Hippo-YAP signaling.
