Growth of GaN films on porous SiC substrate by molecular-beam epitaxy

Porous SiC (PSiC) substrates were used for the growth of GaN by reactive molecular-beam epitaxy with ammonia as the nitrogen source. Improved quality of GaNfilms has been demonstrated for growth on PSiC substrates, as compared to that on standard 6H–SiC substrates. Cross-sectional transmission electron microscopy and electron diffraction showed a reduction in dislocation density and a higher degree of lattice and thermal relaxation in the GaNfilmsgrown on porous substrates. The submicron GaNfilms exhibit a rocking curve linewidth of 3.3 arcmin for (0002) diffraction and 13.7 arcmin for (101̄2) diffraction. Low-temperature photoluminescence showed an excitonic transition with a full width at half maximum of 9.5 meV at 15 K, as well as high quantum efficiency, on the GaN layer grown on PSiC when the thin skin layer on porous SiC was removed before growth

Effectiveness of TiN porous templates on the reduction of threading dislocations in GaN overgrowth by organometallic vapor-phase epitaxy

We report on the reduction of threading dislocations in GaN overlayers grown by organometallic vapor phase epitaxy on micro-porous TiN networks. These networks were obtained by in situannealing of thin Ti layers deposited in a metalization chamber, on the (0001) face of GaN templates. Observations by transmission electron microscopy indicate dislocation reduction by factors of up to 10 in GaN layers grown on TiN networks compared with the control GaN.X-ray diffraction shows that GaNgrown on the TiN network has a smaller (102) plane peak width (4.6 arcmin) than the control GaN (7.8 arcmin). In low temperature photoluminescence spectra, a narrow excitonic full-width-at-half-maximum of 2.4 meV was obtained, as compared to 3.0 meV for the control GaN, confirming the improved crystalline quality of the overgrown GaN layers

Low dislocation densities and long carrier lifetimes in GaN thin films grown on a SiNx nanonetwork

Significant improvement of structural and optical qualities of GaNthin films on sapphire substrates was achieved by metal organic chemical vapor deposition with in situ SiNxnanonetwork. Transmission electron microscope (TEM) studies revealed that screw- and edge-type dislocations were reduced to 4.4×107 and 1.7×107cm−2, respectively, for a ∼5.5-μm-thick layer. Furthermore, room temperature carrier lifetimes of 2.22 and 2.49ns were measured by time-resolved photoluminescence(TRPL) for samples containing single and double SiNx network layers, respectively, representing a significant improvement over the previous studies. The consistent trends among the TEM,x-ray diffraction, and TRPL measurements suggest that in situ SiNx network reduces line defects effectively as well as the point-defect-related nonradiative centers

Efficacy of single and double SiNx interlayers on defect reduction in GaN overlayers grown by organometallic vapor-phase epitaxy

We report on the growth of and evolution of defects in GaN epilayers having single- and double-layer SiNx nanoporous insertion layers. The SiNx was formed in situ in the growth chamber of an organometallic vapor-phase epitaxy system by simultaneous flow of diluted silane and ammonia. The GaN epilayers and SiNx interlayers were grown on 6H-SiC substrates using three different nucleation layers, namely, low-temperature GaN, high-temperature GaN, and high-temperature AlN nucleation layers. X-ray-diffraction rocking curves and cross-sectional and plan-view transmission electron microscope analyses indicated that a nanoporous SiNx layer can reduce the dislocations density in the GaN overgrown layer to ∼3×108cm−2 range; below this level the defect blocking effect of SiNx would saturate. Therefore the insertion of a second SiNx layer becomes much less effective in reducing dislocations, although it continues to reduce the point defects, as suggested by time-resolved photoluminescence measurements. The insertion of SiNx interlayers was found to improve significantly the mechanical strength of the GaN epilayers resulting in a much lower crack line density

Dislocation reduction in GaN grown on porous TiN networks by metal-organic vapor-phase epitaxy

We report on the effectiveness of porous TiN nanonetworks on the reduction of threading dislocations (TDs) in GaN grown by metal-organic vapor-phase epitaxy (MOVPE). The porous TiN networks were formed by in situ annealing of thin-deposited Ti films deposited ex situ on GaN templates within the MOVPE growth chamber. Different annealing parameters in relation to surface porosity of TiN networks were investigated. Transmission electron micrographs indicated dislocation reduction by factors of up to 10 in GaN layers grown on the TiN nanonetwork, compared with a control sample. TiN prevented many dislocations present in the GaN templates from penetrating into the upper layer. Microscale epitaxial lateral overgrowth of GaN above TiN also contributed to TD reduction. The surface porosity of the TiN network had a strong impact on the efficiency of TD reduction. X-ray-diffraction and time-resolved photoluminescence measurements further confirmed the improved GaN quality

The Association of AMPK with ULK1 Regulates Autophagy

Autophagy is a highly orchestrated intracellular bulk degradation process that is activated by various environmental stresses. The serine/threonine kinase ULK1, like its yeast homologue Atg1, is a key initiator of autophagy that is negatively regulated by the mTOR kinase. However, the molecular mechanism that controls the inhibitory effect of mTOR on ULK1-mediated autophagy is not fully understood. Here we identified AMPK, a central energy sensor, as a new ULK1-binding partner. We found that AMPK binds to the PS domain of ULK1 and this interaction is required for ULK1-mediated autophagy. Interestingly, activation of AMPK by AICAR induces 14-3-3 binding to the AMPK-ULK1-mTORC1 complex, which coincides with raptor Ser792 phosphorylation and mTOR inactivation. Consistently, AICAR induces autophagy in TSC2-deficient cells expressing wild-type raptor but not the mutant raptor that lacks the AMPK phosphorylation sites (Ser722 and Ser792). Taken together, these results suggest that AMPK association with ULK1 plays an important role in autophagy induction, at least in part, by phosphorylation of raptor to lift the inhibitory effect of mTOR on the ULK1 autophagic complex

The role of CCN2 in cartilage and bone development

CCN2, a classical member of the CCN family of matricellular proteins, is a key molecule that conducts cartilage development in a harmonized manner through novel molecular actions. During vertebrate development, all cartilage is primarily formed by a process of mesenchymal condensation, while CCN2 is induced to promote this process. Afterwards, cartilage develops into several subtypes with different fates and missions, in which CCN2 plays its proper roles according to the corresponding microenvironments. The history of CCN2 in cartilage and bone began with its re-discovery in the growth cartilage in long bones, which determines the skeletal size through the process of endochondral ossification. CCN2 promotes physiological developmental processes not only in the growth cartilage but also in the other types of cartilages, i.e., Meckel’s cartilage representing temporary cartilage without autocalcification, articular cartilage representing hyaline cartilage with physical stiffness, and auricular cartilage representing elastic cartilage. Together with its significant role in intramembranous ossification, CCN2 is regarded as a conductor of skeletogenesis. During cartilage development, the CCN2 gene is dynamically regulated to yield stage-specific production of CCN2 proteins at both transcriptional and post-transcriptional levels. New functional aspects of known biomolecules have been uncovered during the course of investigating these regulatory systems in chondrocytes. Since CCN2 promotes integrated regeneration as well as generation (=development) of these tissues, its utility in regenerative therapy targeting chondrocytes and osteoblasts is indicated, as has already been supported by experimental evidence obtained in vivo

Translational Up-Regulation and High-Level Protein Expression from Plasmid Vectors by mTOR Activation via Different Pathways in PC3 and 293T Cells

BACKGROUND: Though 293T cells are widely used for expression of proteins from transfected plasmid vectors, the molecular basis for the high-level expression is yet to be understood. We recently identified the prostate carcinoma cell line PC3 to be as efficient as 293T in protein expression. This study was undertaken to decipher the molecular basis of high-level expression in these two cell lines. METHODOLOGY/PRINCIPAL FINDINGS: In a survey of different cell lines for efficient expression of platelet-derived growth factor-B (PDGF-B), β-galactosidase (β-gal) and green fluorescent protein (GFP) from plasmid vectors, PC3 was found to express at 5-50-fold higher levels compared to the bone metastatic prostate carcinoma cell line PC3BM and many other cell lines. Further, the efficiency of transfection and level of expression of the reporters in PC3 were comparable to that in 293T. Comparative analyses revealed that the high level expression of the reporters in the two cell lines was due to increased translational efficiency. While phosphatidic acid (PA)-mediated activation of mTOR, as revealed by drastic reduction in reporter expression by n-butanol, primarily contributed to the high level expression in PC3, multiple pathways involving PA, PI3K/Akt and ERK1/2 appear to contribute to the abundant reporter expression in 293T. Thus the extent of translational up-regulation attained through the concerted activation of mTOR by multiple pathways in 293T could be achieved through its activation primarily by the PA pathway in PC3. CONCLUSIONS/SIGNIFICANCE: Our studies reveal that the high-level expression of proteins from plasmid vectors is effected by translational up-regulation through mTOR activation via different signaling pathways in the two cell lines and that PC3 is as efficient as 293T for recombinant protein expression. Further, PC3 offers an advantage in that the level of expression of the protein can be regulated by simple addition of n-butanol to the culture medium

Regulation of TFEB and V-ATPases by mTORC1

TORC1 is a key regulator of cell growth in response to nutrients and acts at the surface of the late endosome. This study identifies V-ATPase genes as transcriptional targets of TORC1 and implicates the transcription factor TFEB as an important mediator of TORC1-dependent gene expression and TORC1-regulated endocytosis