2D polyaniline with exchangeable interlayer fluid for fast and stable volumetric dual ion storage

Two-dimensional(2D) layered materials are widely applied in energy devices including lithium-ion battery and supercapacitor due to their unique properties,such as tunable interlayer structure,numerous active sites,large aspect ratio versatile interlayer chemistry.In this work,2D layered tungstate acidlinked polyaniline(TALP) presented a fluid-in-solid structure,which allowed facile exchange of the interlayer fluid from moisture to conventional Li^(+) containing electrolyte.With fast and stable dual ion storage(Li^(+) and PF_(6)^(-)),TALP demonstrates high-rate volumetric capacity(39 mAh cm_(-3) at 2000 mA g^(-1)) and good stability(2000 cycles at 200 mA g^(-1)) within the working potential window of 1.5-4.5 V versus Li^(+)/Li.

Junction plakoglobin regulates and destabilizes HIF2α to inhibit tumorigenesis of renal cell carcinoma

Background:Increased hypoxia-inducible factor 2α(HIF2α)activation is a common event in clear cell renal cell carcinoma(ccRCC)progression.However,the function and underlying mechanism of HIF2α in ccRCC remains uninvestigated.We conducted this study to access the potential link between junction plakoglobin(JUP)and HIF2αin ccRCC.Methods:Affinity purification and mass spectrometry(AP-MS)screening,glutathione-s-transferase(GST)pull-down and co-immunoprecipitation(Co-IP)assays were performed to detect the interacting proteins of HIF2α.Quantitative PCR(qPCR)and Western blotting were used to detect the expression of JUP in human ccRCC samples.Luciferase reporter assays,chromatin immunoprecipitation(ChIP),cycloheximide chase assays,and ubiquitination assays were conducted to explore the regulation of JUP on the activity of HIF2α.Cell Counting Kit-8(CCK-8)assays,colony formation assays,transwell assays,and xenograft tumor assays were performed to investigate the effect of JUP knockdown or overexpression on the tumorigenicity of renal cancer cells.Results:We identified JUP as a novel HIF2α-binding partner and revealed an important role of JUP in recruiting von Hippel-Lindau(VHL)and histone deacetylases 1/2(HDAC1/2)to HIF2α to regulate its stability and transactivation.JUP knockdown promoted and overexpression suppressed the tumorigenicity of renal cell carcinoma in vitro and in vivo.Importantly,the low expression of JUP was found in clinical ccRCC samples and correlated with enhanced hypoxia scores and poor treatment outcomes.Conclusion:Taken together,these data support a role of JUP in modulating HIF2α signaling during ccRCC progression and identify JUP as a potential therapeutic target.