A Near-Infrared Study of the Highly-Obscured Active Star-Forming Region W51B

We present wide-field JHKs-band photometric observations of the three compact HII regions G48.9-0.3, G49.0-0.3, and G49.2-0.3 in the active star-forming region W51B. The star clusters inside the three compact HII regions show the excess number of stars in the J-Ks histograms compared with reference fields. While the mean color excess ratio E(J-H)/E(H-Ks) of the three compact HII regions are similar to ~ 2.07, the visual extinctions toward them are somewhat different: ~ 17 mag for G48.9-0.3 and G49.0-0.3; ~ 23 mag for G49.2-0.3. Based on their sizes and brightnesses, we suggest that the age of each compact HII region is =< 2 Myr. The inferred total stellar mass, ~ 1.4 x 10^4 M_sun, of W51B makes it one of the most active star forming regions in the Galaxy with the star formation efficiency of ~ 10 %.Comment: 12 pages, 10 eps figures, uses jkas.st

Transcriptional Co-repressor Function of the Hippo Pathway Transducers YAP and TAZ

SummaryYAP (yes-associated protein) and TAZ are oncogenic transcriptional co-activators downstream of the Hippo tumor-suppressor pathway. However, whether YAP and/or TAZ (YAP/TAZ) engage in transcriptional co-repression remains relatively unexplored. Here, we directly demonstrated that YAP/TAZ represses numerous target genes, including tumor-suppressor genes such as DDIT4 (DNA-damage-inducible transcript 4) and Trail (TNF-related apoptosis-inducing ligand). Mechanistically, the repressor function of YAP/TAZ requires TEAD (TEA domain) transcription factors. A YAP/TAZ-TEAD complex recruits the NuRD complex to deacetylate histones and alters nucleosome occupancy at target genes. Functionally, repression of DDIT4 and Trail by YAP/TAZ is required for mTORC1 (mechanistic target of rapamycin complex 1) activation and cell survival, respectively. Our demonstration of the transcriptional co-repressor activity of YAP/TAZ opens a new avenue for understanding the Hippo signaling pathway

Near-Infrared Spectroscopy of Infrared-Excess Stellar Objects in the Young Supernova Remnant G54.1+0.3

We present the results of broadband near-infrared spectroscopic observations of the recently discovered mysterious stellar objects in the young supernova remnant G54.1+0.3. These objects, which show significant mid-infrared-excess emission, are embedded in a diffuse loop structure of ~1' in radius. Their near-infrared spectra reveal characteristics of late O- or early B-type stars with numerous H and He I absorption lines, and we classify their spectral types to be between O9 and B2 based on an empirical relation derived here between the equivalent widths of the H lines and stellar photospheric temperatures. The spectral types, combined with the results of spectral energy distribution fits, constrain the distance to the objects to be 6.0 ± 0.4 kpc. The photometric spectral types of the objects are consistent with those from the spectroscopic analyses, and the extinction distributions indicate a local enhancement of matter in the western part of the loop. If these objects originate via triggered formation by the progenitor star of G54.1+0.3, then their formations likely began during the later evolutionary stages of the progenitor, although a rather earlier formation may still be possible. If the objects and the progenitor belong to the same cluster of stars, then our results constrain the progenitor mass of G54.1+0.3 to be between 18 and ~35 M_☉ and suggest that G54.1+0.3 was either a Type IIP supernova or, with a relatively lower possibility, Type Ib/c from a binary system

Discovery of a rapid, luminous nova in NGC 300 by the KMTNet Supernova Program

We present the discovery of a rapidly evolving transient by the Korean Microlensing Telescope Network Supernova Program (KSP). KSP is a novel high-cadence supernova survey that offers deep ($\sim21.5$ mag in $BVI$ bands) nearly continuous wide-field monitoring for the discovery of early and/or fast optical transients. KSP-OT-201509a, reported here, was discovered on 2015 September 27 during the KSP commissioning run in the direction of the nearby galaxy NGC~300, and stayed above detection limit for $\sim$ 22 days. We use our $BVI$ light-curves to constrain the ascent rate, $-3.7(7)$ mag day$^{-1}$ in $V$, decay time scale, $t^{V}_{2}=1.7(6)$ days, and peak absolute magnitude, $-9.65\leq M_{V}\leq -9.25$ mag. We also find evidence for a short-lived pre-maximum halt in all bands. The peak luminosity and lightcurve evolution make KSP-OT-201509a consistent with a bright, rapidly decaying nova outburst. We discuss constraints on the nature of the progenitor and its environment using archival HST/ACS images and conclude with a broad discussion on the nature of the system.Comment: 7 pages in aastex6 two-column format, 4 figures; accepted in Ap

Cellular energy stress induces AMPK-mediated regulation of YAP and the Hippo pathway.

YAP (Yes-associated protein) is a transcription co-activator in the Hippo tumour suppressor pathway and controls cell growth, tissue homeostasis and organ size. YAP is inhibited by the kinase Lats, which phosphorylates YAP to induce its cytoplasmic localization and proteasomal degradation. YAP induces gene expression by binding to the TEAD family transcription factors. Dysregulation of the Hippo-YAP pathway is frequently observed in human cancers. Here we show that cellular energy stress induces YAP phosphorylation, in part due to AMPK-dependent Lats activation, thereby inhibiting YAP activity. Moreover, AMPK directly phosphorylates YAP Ser 94, a residue essential for the interaction with TEAD, thus disrupting the YAP-TEAD interaction. AMPK-induced YAP inhibition can suppress oncogenic transformation of Lats-null cells with high YAP activity. Our study establishes a molecular mechanism and functional significance of AMPK in linking cellular energy status to the Hippo-YAP pathway

KIOM-79, an Inhibitor of AGEs–Protein Cross-linking, Prevents Progression of Nephropathy in Zucker Diabetic Fatty Rats

Advanced glycation end products (AGEs) have been implicated in the development of diabetic complications, including diabetic nephropathy. KIOM-79, an 80% ethanolic extract obtained from parched Puerariae Radix, gingered Magnolia Cortex, Glycyrrhiza Radix and Euphorbia Radix, was investigated for its effects on the development of renal disease in Zucker diabetic fatty rats, an animal model of type 2 diabetes. In vitro inhibitory effect of KIOM-79 on AGEs cross-linking was examined by enzyme-linked immunosorbent assay (ELISA). KIOM-79 (50 mg/kg/day) was given to Zucker diabetic fatty rats for 13 weeks. Body and kidney weight, blood glucose, glycated hemoglobin, urinary albumin and creatinine excretions were monitored. Kidney histopathology, collagen accumulation, fibrinogen and transforming growth factor-beta 1 (TGF-β1) expression were also examined. KIOM-79 reduced blood glucose, kidney weight, histologic renal damage and albuminuria in Zucker diabetic fatty rats. KIOM-79 prevented glomerulosclerosis, tubular degeneration, collagen deposition and podocyte apoptosis. In the renal cortex, TGF-β1, fibronectin mRNA and protein were significantly reduced by KIOM-79 treatment. KIOM-79 reduces AGEs accumulation in vivo, AGE–protein cross-linking and protein oxidation. KIOM-79 could be beneficial in preventing the progression of diabetic glomerularsclerosis in type 2 diabetic rats by attenuating AGEs deposition in the glomeruli