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H2A.Z is a histone variant that provides specific structural and docking-side properties to the nucleosome, resulting in diverse and specialised molecular and cellular functions. In this review, we discuss the latest studies uncovering new functional aspects of mammalian H2A.Z in gene transcription, including pausing and elongation of RNA polymerase II (RNAPII) and enhancer activity; DNA repair; DNA replication; and 3D chromatin structure. We also review the recently described role of H2A.Z in embryonic development, cell differentiation, neurodevelopment, and brain function. In conclusion, our cumulative knowledge of H2A.Z over the past 40 years, in combination with the implementation of novel molecular technologies, is unravelling an unexpected and complex role of histone variants in gene regulation and disease. The histone variant H2A.Z has been involved in many diverse and contrasting functions. H2A.Z complex biology, including different post-translational modifications, isoforms, and nucleosome partners, may explain the conflicting molecular properties associated with H2A.Z, however, how all these molecular layers work together remains unclear. H2A.Z is essential for RNA polymerase II pausing and enhancer activation during transcription, as well as initiation of replication origins, accurate mitotic transition, and repair at DNA damaged sites. H2A.Z is a master regulator for development, cell differentiation, and neural activity; therefore, we predict that future studies will link H2A.Z with a range of neurological and developmental disorders. [ABSTRACT FROM AUTHOR]

Vitamin K was discovered fortuitously in 1929 as part of experiments on sterol metabolism and was immediately associated with blood coagulation. In the decade that followed, the principal K vitamers, phylloquinone and the menaquinones, were isolated and fully characterized. In the early 1940s, the first vitamin K antagonists were discovered and crystallized with one of its derivatives, warfarin, still being widely used in today's clinical setting. However, major progress in our understanding of the mechanisms of action of vitamin K came in the 1970s with the discovery of γ-carboxyglutamic acid (Gla), a new amino acid common to all vitamin K proteins. This discovery not only provided the basis to understanding earlier findings about prothrombin but later led to the discovery of vitamin K-dependent proteins (VKDPs) not involved in hemostasis. The 1970s also saw an important breakthrough with respect to our understanding of the vitamin K cycle and marked the discovery of the first bone VKDP, osteocalcin. Important studies relating to the role of vitamin K in sphingolipid synthesis were also underway at that time and would pave the way to further work 15 years later. The decades that followed saw the discovery of additional VKDPs showing wide tissue distribution and functional scope, the latest members having been identified in 2008. The 1990s and 2000s were also marked by important epidemiological and intervention studies that focused on the translational impact of recent vitamin K discoveries, notably with respect to bone and cardiovascular health. This short review presents an overview of the history of vitamin K and of its recent developments. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

An introduction is presented in which the editor discusses various reports within the issue on topics which highlights the diversity and complexity associated with structures and functions of complement proteins (C1q) and C1q family members.