Equity market volatility and expected risk premium

This paper revisits the time-series relation between the conditional risk premium and variance of the equity market portfolio. The main innovation is that we construct a measure of the ex ante equity market risk premium using corporate bond yield spread data. This measure is forward-looking and does not rely critically on either realized equity returns or instrumental variables. We find strong support for a positive risk-return tradeoff, and this result is not sensitive to a number of robustness checks, including alternative proxies of the conditional stock variance and controls for hedging demands.Stock exchanges ; Securities

Induction of MET Receptor Tyrosine Kinase Down-Regulation through Antibody-Mediated Receptor Clustering

The proto-oncoprotein MET is a receptor tyrosine kinase that plays a key role in cancer cell growth and invasion. We have used fluorescence-tagged antibodies to activate MET in live serum-starved glioblastoma cells and monitor the fate of antibody-bound MET receptor in single cell-based assays. We found that the antibodies induced rapid and transient formation of highly polarized MET clusters on the plasma membrane and promoted the activation of MET, resembling the initial effects of binding to its ligand, HGF. However, the antibody-induced clustering and activation of MET led to the rapid removal of the receptor from cell surface and altered its intracellular processing, resulted in rapid degradation of the receptor. Consequently, while cells pre-treated with HGF remain competent to respond to further HGF stimulation, cells pre-treated with antibodies are refractory to further HGF stimulation due to antibody-mediated MET depletion. Removal of MET by sustained treatment of antibodies blocked cancer cell migration and invasion. Our studies reveal a novel mechanism to alter the recycling process of MET in glioblastoma cancer cells by promoting the receptor degradation through a proteasome-sensitive and lysosome-dependent pathway through the ligand-independent activation of MET using anti-MET antibodies

Methylated DNMT1 and E2F1 Are Targeted for Proteolysis by L3MBTL3 and CRL4DCAF5 Ubiquitin Ligase

Many non-histone proteins are lysine methylated and a novel function of this modification is to trigger the proteolysis of methylated proteins. Here, we report that the methylated lysine 142 of DNMT1, a major DNA methyltransferase that preserves epigenetic inheritance of DNA methylation patterns during DNA replication, is demethylated by LSD1. A novel methyl-binding protein, L3MBTL3, binds the K142-methylated DNMT1 and recruits a novel CRL4DCAF5 ubiquitin ligase to degrade DNMT1. Both LSD1 and PHF20L1 act primarily in S phase to prevent DNMT1 degradation by L3MBTL3-CRL4DCAF5. Mouse L3MBTL3/MBT-1 deletion causes accumulation of DNMT1 protein, increased genomic DNA methylation, and late embryonic lethality. DNMT1 contains a consensus methylation motif shared by many non-histone proteins including E2F1, a key transcription factor for S phase. We show that the methylation-dependent E2F1 degradation is also controlled by L3MBTL3-CRL4DCAF5. Our studies elucidate for the first time a novel mechanism by which the stability of many methylated non-histone proteins are regulated

One-way cloak based on nonreciprocal photonic crystal

We propose a physical concept of non-reciprocal transformation optics, by which a one-way invisible cloak is designed. The one-way invisible cloak is made of a coordinate-transformed nonreciprocal photonic crystal, showing a perfect cloaking for wave incident from one direction but acting as a perfect reflector for wave from the counter direction. The proposed design shows a high promise of applications in military, as protecting the own information to be detected but efficiently grabbing the information from the “enemy” side

Traffic-Aware Transmission Mode Selection in D2D-enabled Cellular Networks with Token System

We consider a D2D-enabled cellular network where user equipments (UEs) owned by rational users are incentivized to form D2D pairs using tokens. They exchange tokens electronically to "buy" and "sell" D2D services. Meanwhile the devices have the ability to choose the transmission mode, i.e. receiving data via cellular links or D2D links. Thus taking the different benefits brought by diverse traffic types as a prior, the UEs can utilize their tokens more efficiently via transmission mode selection. In this paper, the optimal transmission mode selection strategy as well as token collection policy are investigated to maximize the long-term utility in the dynamic network environment. The optimal policy is proved to be a threshold strategy, and the thresholds have a monotonicity property. Numerical simulations verify our observations and the gain from transmission mode selection is observed.Comment: 7 pages, 6 figures. A shorter version is submitted to EUSIPC