HERV reactivation by adenovirus infection is associated with viral immune regulation.

Human endogenous retroviruses (HERVs), which are normally silenced by methylation or mutation, can be reactivated by a variety of environmental factors, including infection with exogenous viruses. In this work, we investigated the transcriptional activity of HERVs following infection of human liver cells (HepaRG) with human adenovirus C serotype 5 (HAdV-C5). HAdV-C5 infection results in reactivation of several HERV groups as well as differentially expressed genes.

Accessing Homo- and Heterobimetallic Complexes with a Dianionic Pentadentate Ligand.

The tetrapyrazolylpyridyl diborate (BPzPy) ligand provides a suitable platform for the isolation of heterobimetallic main-group element compounds as well as homotetrametallic copper complexes. The heterobimetallic tin(II)-lithium(I) () and tin(II)-thallium(I) () complexes have been synthesized, isolated, and fully characterized including single-crystal X-ray diffraction analysis. When reacted with copper(I) sources, complex grants access to a homotetrametallic copper(I) complex ().

DEAD-box ATPase Dbp2 is the key enzyme in an mRNP assembly checkpoint at the 3'-end of genes and involved in the recycling of cleavage factors.

mRNA biogenesis in the eukaryotic nucleus is a highly complex process. The numerous RNA processing steps are tightly coordinated to ensure that only fully processed transcripts are released from chromatin for export from the nucleus. Here, we present the hypothesis that fission yeast Dbp2, a ribonucleoprotein complex (RNP) remodelling ATPase of the DEAD-box family, is the key enzyme in an RNP assembly checkpoint at the 3'-end of genes.

Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.

Merkel cell polyomavirus (MCPyV) is the causative agent of the majority of Merkel cell carcinomas (MCC). The virus has limited coding capacity, with its early viral proteins, large T (LT) and small T (sT), being multifunctional and contributing to infection and transformation. A fundamental difference in early viral gene expression between infection and MCPyV-driven tumorigenesis is the expression of a truncated LT (LTtr) in the tumor.