Transforming growth factor ␤ (TGF-␤) is a potent multifunctional regulator of cell growth and differentiation. Although nearly all cells synthesize and respond to TGF-␤, bone and cartilage are particularly rich in this growth factor (6, 46). TGF-␤1, the prototypic member of the TGF-␤ superfamily, elicits diverse cellular responses, including (i) inhibition of adipogenesis and myogenesis and (ii) stimulation of chondrogenesis and osteogenesis (31). TGF-␤1 stimulates the synthesis of matrix proteins and their receptors (for example, fibronectin, fibronectin receptor, collagen, osteonectin, osteopontin, and integrins) and inhibits matrix degradation by increasing the production of protease inhibitors and decreasing the production of proteases (42). Members of the TGF-␤ superfamily with important effects on bone cell differentiation are bone morphogenetic proteins (BMPs) (17, 41), which were first identified as factors that induce bone formation in vivo when implanted into muscular tissues (54). Unlike TGF-␤, which induces new bone formation only when injected near bone, BMPs produce bone formation even when injected into ectopic sites. TGF-␤ and BMPs bind to distinct receptors, TGF-␤ type I and II receptors for TGF-␤ and BMP type I and II receptors for BMPs. Following ligand binding, the receptor-associated kinase is activated and phosphorylates Smads, which move into the nucleus to stimulate the transcription of a set of target genes. Smad2 and -3 are activated by TGF-␤ receptors and mediate TGF-␤ responses, whereas Smad1, -5, and -8 are activated by BMP receptors and transduce BMP signals (15,32,57).The pluripotent mesenchymal precursor cell line C2C12 provides a model system to study the early stage of osteoblast differentiation during bone formation in muscular tissues. In this model, TGF-␤1 inhibits the differentiation of C2C12 cells into multinucleated myotubes without inducing osteoblast phenotypes. BMP-2 not only inhibits the terminal differentiation of C2C12 cells but also induces osteoblast phenotypes (20). Therefore, the C2C12 model is useful for analyzing both the common and specific signaling mechanisms of TGF-␤ and BMPs. In C2C12 cells, overexpression of Smad1 and Smad5 induced alkaline phosphatase (ALP) activity, a typical osteoblast-specific marker, and inhibited muscle-specific gene expression (11,36,56). These results suggested that BMP functions via either Smad1 or Smad5 and that the induction of the osteoblast phenotype and the inhibition of myogenic differentiation are regulated at the transcriptional level. However, the molecular mechanisms through which Smads block myogenic differentiation and induce osteogenic differentiation are not known.Runx/PEBP2/Cbf (hereafter referred to as Runx) is a sequence-specific DNA binding protein that recognizes a specific DNA sequence originally identified as the binding site for

Electrode designs, which can accommodate severe volume changes (ca. 400 %) of silicon anode materials upon lithium insertion, are the main prerequisite for high-performance lithium ion batteries. Among various techniques investigated for this purpose, a robust polymeric binder is a promising means to inhibit mechanical fracture of silicon negative electrodes during cycling.Lithium ion batteries (LIBs) are one of the most promising energy storage devices owing to their high power and energy densities. [1] For LIBs, silicon is a promising candidate anode material owing to its high theoretical specific capacity of 4200 mAh g À1 for Li 4.4 Si, low electrochemical potential between 0 and 0.4 V versus Li/Li + , and small initial irreversible capacity compared with other metal-or alloy-based anode materials. [2] Nevertheless, the practical application of silicon to LIBs is still quite challenging because silicon suffers from severe volume changes (ca. 400 %) during Li + insertion and extraction processes, which breaks electrical contact between the silicon particles and results in degradation of electrodes and rapid capacity loss. [3] To alleviate volume change, silicon nanoparticles and porous silicon materials have been extensively studied because the smaller particles undergo smaller absolute volume change. [4] The aggregation of silicon particles upon cycling, however, accelerates the degradation of electrodes. Thus, many efforts have focused on the synthesis of silicon-carbon composites to prevent the agglomeration of silicon, resulting in a highly improved cycle performance. [5] Although remarkable improvements in the electrochemical performance of silicon-based anodes have been achieved, electrode deformation and external cell expansion still occur because of the inherent volume change of silicon. This large cell volume change is the main factor limiting the commercialization of silicon-based anode materials.

Particle‐larly good! Thermal annealing and etching of physical composite butyl‐capped Si gels and SiO2 nanoparticles at 900 °C under an Ar atmosphere is a versatile method for the formation of 3D porous bulk Si particles (see picture). Complete etching of the SiO2 from the SiO2/carbon‐coated Si (c‐Si) composite results in the retention of the remaining c‐Si as a highly porous but interconnected structure, which preserves the starting morphology.

Please note that Figure 3 should read as follows (left-hand segment 24 and not 14; right-hand segment 37 and not 26): Figure 3. Venn diagram of proteins overlapping between the two trials and the number of proteins identified in each trial. Of the total proteins from the first and second trials, 76.9 and 68.4%, respectively, were common to both trials.

A series of transcription factors critical for maintenance of the neural stem cell state have been identified, but the role of functionally important corepressors in maintenance of the neural stem cell state and early neurogenesis remains unclear. Previous studies have characterized the expression of both SMRT (also known as NCoR2, nuclear receptor co-repressor 2) and NCoR in a variety of developmental systems; however, the specific role of the SMRT corepressor in neurogenesis is still to be determined. Here we report a critical role for SMRT in forebrain development and in maintenance of the neural stem cell state. Analysis of a series of markers in SMRT-gene-deleted mice revealed the functional requirement of SMRT in the actions of both retinoic-acid-dependent and Notch-dependent forebrain development. In isolated cortical progenitor cells, SMRT was critical for preventing retinoic-acid-receptor-dependent induction of differentiation along a neuronal pathway in the absence of any ligand. Our data reveal that SMRT represses expression of the jumonji-domain containing gene JMJD3, a direct retinoic-acid-receptor target that functions as a histone H3 trimethyl K27 demethylase and which is capable of activating specific components of the neurogenic program.