Alpha2-antiplasmin deficiency affects depression and anxiety-like behavior and apoptosis induced by stress in mice.

Objectives: Depression is a psychiatric disorder that affects about 10% of the world's population and is accompanied by anxiety. Depression and anxiety are often caused by various stresses. However, the etiology of depression and anxiety remains unknown.

Distinct roles for U-type proteins in iron-sulfur cluster biosynthesis revealed by genetic analysis of the Bacillus subtilis sufCDSUB operon.

The biosynthesis of iron-sulfur (Fe-S) clusters in Bacillus subtilis is mediated by the SUF-like system composed of the sufCDSUB gene products. This system is unique in that it is a chimeric machinery comprising homologues of E. coli SUF components (SufS, SufB, SufC and SufD) and an ISC component (IscU).

Zinc-Ligand Swapping Mediated Complex Formation and Sulfur Transfer between SufS and SufU for Iron-Sulfur Cluster Biogenesis in Bacillus subtilis.

SufU is a zinc-containing protein involved in mobilization of sulfur from SufS for iron-sulfur cluster biogenesis of Bacillus subtilis. Structural basis for the sulfur transfer in SufS-SufU complex was revealed. A zinc-ligand exchange reaction upon SufS-SufU complexation provides a free thiol from Cys41 of SufU as a sulfur acceptor.

α2-antiplasmin modulates bone formation by negatively regulating osteoblast differentiation and function.

α2-antiplasmin (α2AP) is known to be a physiological inhibitor of plasmin. Previously, we showed that α2AP displays various functions, such as promotion of extracellular matrix production, cell growth, and cell differentiation that are not promoted by its function as a plasmin inhibitor. We herein investigated the role of α2AP in bone formation by examining calcein incorporation after its injection in α2AP-deficient mice.

uPA-derived peptide, Å6 is involved in the suppression of lipopolysaccaride-promoted inflammatory osteoclastogenesis and the resultant bone loss.

Introduction: Chronic inflammatory diseases such as rheumatoid arthritis and periodontitis frequently cause bone destruction. Inflammation-induced bone loss results from the increase of bone-resorbing osteoclasts. Recently, we demonstrated that urokinase type plasminogen activator (uPA) suppressed lipopolysaccaride (LPS)-inflammatory osteoclastogenesis through the adenosine monophosphate-activated protein kinase (AMPK) pathway, whereas its receptor (uPAR) promoted that through the Akt pathway.