Every cell is enclosed by a thin double layer of lipids that separates the distinct internal environment of the cell from the extracellular space. Damage to this lipid bilayer, also referred to as plasma membrane, disturbs the cellular functions and may lead to the death of the cell. For example, downhill walking tears many little holes into the plasma membranes of the muscle cells in our legs. To prevent irreparable damage, muscle cells have efficient systems to seal these holes again. Researchers at Karlsruhe Institute of Technology (KIT) and Heidelberg University have succeeded for the first time in observing membrane repair in real-time in a living organism.

Fossils from two caves in south-west China have revealed a previously unknown Stone Age people and give a rare glimpse of a recent stage of human evolution with startling implications for the early peopling of Asia.

A research team has identified epigenetic signatures, markers on DNA that control transient changes in gene expression, within reprogrammed skin cells. These signatures can predict the expression of a wound-healing protein in reprogrammed skin cells or induced pluripotent stem cells (iPSCs), cells that take on embryonic stem cell properties. Understanding how the expression of the protein is controlled brings us one step closer to developing personalized tissue regeneration strategies using stem cells from a patient, instead of using human embryonic stem cells. The study was published in the Journal of Cell Science.

A Loyola University Chicago Stritch School of Medicine study has revealed details of the complex molecular process involving a protein that enables cancer cells to establish tumors in distant parts of the body.

A team of researchers led by scientists at The Rockefeller University has identified a novel mechanism by which influenza interferes with antiviral host response. The finding, reported in this week's issue of the journal Nature, shows that the immunosuppressive NS1 protein of the influenza A virus hijacks key regulators of antiviral gene function by mimicking a core component of gene regulating machinery. The results they describe have major implications for our understanding of the biology of seasonal influenza virus and its pathogenesis. This research also suggests a possible target for a new class of antiviral and anti-inflammatory drugs.