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Transcriptional enhanced associate domain (TEAD) transcription factors play important roles during development, cell proliferation, regeneration, and tissue homeostasis. TEAD integrates with and coordinates various signal transduction pathways including Hippo, Wnt, transforming growth factor beta (TGFβ), and epidermal growth factor receptor (EGFR) pathways. TEAD deregulation affects well-established cancer genes such as KRAS, BRAF, LKB1, NF2, and MYC, and its transcriptional output plays an important role in tumor progression, metastasis, cancer metabolism, immunity, and drug resistance. To date, TEADs have been recognized to be key transcription factors of the Hippo pathway. Therefore, most studies are focused on the Hippo kinases and YAP/TAZ, whereas the Hippo-dependent and Hippo-independent regulators and regulations governing TEAD only emerged recently. Deregulation of the TEAD transcriptional output plays important roles in tumor progression and serves as a prognostic biomarker due to high correlation with clinicopathological parameters in human malignancies. In addition, discovering the molecular mechanisms of TEAD, such as post-translational modifications and nucleocytoplasmic shuttling, represents an important means of modulating TEAD transcriptional activity. Collectively, this review highlights the role of TEAD in multistep-tumorigenesis by interacting with upstream oncogenic signaling pathways and controlling downstream target genes, which provides unprecedented insight and rationale into developing TEAD-targeted anticancer therapeutics.

Metal–organic polyhedra (MOPs) are comprehensively summarized and classified based on topology, providing new directions for MOP design and forthcoming applications.

Nowadays, the exploration of zinc oxide nanoparticles (ZnO NPs) based products is booming in the various directions of bio-nanomedicine and other consumer products, but the comprehensive toxicological impact posed by ZnO NPs still remains unclear. The present study systematically investigates and correlates the toxicity evaluation of ZnO NPs in RAW 264.7 murine macrophages (in vitro) and male ICR mice (in vivo) by two different administration routes, i.e. g.i. and i.p. at different doses. The in vitro studies showed a slight rise in intracellular reactive oxygen species level (ROS), NF-kB transcription factor expression (TF) and NPs uptake at higher dose, indicating the non-toxic nature of ZnO NPs below 100 mg mL À1 doses. The in vivo results demonstrate a slight gain in body weight (BW), reduction in the organ weight, mild to severe pathological alteration in the organs depending upon NP dosage and mode of administration routes. The histopathological investigation suggests that the liver, kidney, lung, spleen, and pancreas may be the target organs for ZnO NPs according to the administration routes. Serum biochemistry assay shows an elevation in the GPT and ALP level, suggesting liver dysfunction. To our knowledge, this is the first study to report the toxic effects of ZnO NPs through i.p. administration.Further, the present work will offer a deeper understanding regarding the toxicology and in vivo behaviours of ZnO NPs in mice depending upon the various administration routes. † Electronic supplementary information (ESI) available: Supplementary Fig. 1 shows the TEM images of (A) bare ZnO NPs, (B) aminated ZnO NPs showing a thin lm coated on the ZnO surfaces, and (C) the surface charges of the bare and aminated ZnO NPs in aqueous solution at different pH measured by zeta potentiometer. Supplementary Fig. 2 shows the cellular uptake behavior of ZnO NPs. Supplementary Fig.3 shows the gross observation of mice aer intraperitoneal administration of 100 mg mL À1 ZnO nanoparticles. See

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Although the organic light‐emitting diode (OLED) has been successfully commercialized, the development of deep‐blue OLEDs with high efficiency and long lifetime remains a challenge. Here, a novel hyperfluorescent OLED that incorporates the Pt(II) complex (PtON7‐dtb) as a phosphorescent sensitizer and a hydrocarbon‐based and multiple resonance‐based fluorophore as an emitter (TBPDP and ν‐DABNA) in the device emissive layer (EML), is proposed. Such an EML system can promote efficient energy transfer from the triplet excited states of the sensitizer to the singlet excited states of the fluorophore, thus significantly improving the efficiency and lifetime of the device. As a result, a deep‐blue hyperfluorescent OLED using a multiple resonance‐based fluorophore (ν‐DABNA) with Commission Internationale de L'Eclairage chromaticity coordinate y below 0.1 is demonstrated, which attains a narrow full width at half maximum of ≈17 nm, fourfold increased maximum current efficiency of 48.9 cd A−1, and 19‐fold improved half‐lifetime of 253.8 h at 1000 cd m−2 compared to a conventional phosphorescent OLED. The findings can lead to better understanding of the hyperfluorescent OLEDs with high performance.

We demonstrate that dramatically improved hole injection can be achieved by inserting a very thin C60 film between the indium tin oxide (ITO) electrode and N,N′-diphenyl-N,N′-bis(1,1′-biphenyl)-4,4′-diamine (NPB) layer. This result is ascribed to the formation of an interfacial dipole layer of buckminsterfullerene (C60) on the ITO electrode. The dipole layer induces the surface potential shift that contributes to improve the charge injection efficiency. The chemical shift was downward to help lower the hole injection energy barrier from the ITO electrode to the NPB layer, consistent with the moderately strong electron accepting nature of C60. The enhanced-charge injection provides a simple way of reducing the power consumption of organic electronic devices for real applications.

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