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Host cell membrane-trafficking pathways are often manipulated by bacterial pathogens to gain cell entry, avoid immune responses, or to obtain nutrients. The 1,369-residue OtDUB protein from the obligate intracellular human pathogen Orientia tsutsugamushi bears a deubiquitylase (DUB) and additional domains. Here we show that OtDUB ectopic expression disrupts membrane trafficking through multiple mechanisms. OtDUB binds directly to the clathrin adaptor-protein (AP) complexes AP-1 and AP-2, and the OtDUB(275–675) fragment is sufficient for binding to either complex. To assess the impact of OtDUB interactions with AP-1 and AP-2, we examined trans-Golgi trafficking and endocytosis, respectively. Endocytosis is reduced by two separate OtDUB fragments: one contains the AP-binding domain (OtDUB(1–675)), and the other does not (OtDUB(675–1369)). OtDUB(1–675) disruption of endocytosis requires its ubiquitin-binding capabilities. OtDUB(675–1369) also fragments trans- and cis-Golgi structures. Using a growth-based selection in yeast, we identified viable OtDUB(675–1369) point mutants that also no longer caused Golgi defects in human cells. In parallel, we found OtDUB(675–1369) binds directly to phosphatidylserine, and this lipid binding is lost in the same mutants. Together these results show that OtDUB contains multiple activities capable of modulating membrane trafficking. We discuss how these activities may contribute to Orientia infections.

We investigated the effect of picosecond pulsed laser irradiation on the sheet resistance and microstructure of the silver nanowire films coated on PET substrates. The sheet resistance of the silve...

We have investigated the effect of plasma-induced damages on the electron transport layers in organic light-emitting devices. Tris(8-hydroxyquinolinato) aluminum, tris(2,4,6-trimethyl-3-(pyridine-3yl)phenyl) borane, and 3-(4-biphenyl)-4-phenyl-5-tert-butylphenyl-1,2,4-triazole (TAZ) layers were used for studying plasma-induced degradation of electron transport materials. The thicknesses, photoluminescence spectra and the current-voltage curves of organic electron transport materials were measured after exposing to Ar plasma. The high-energy species in plasma induce the sputtering of organic layers, quenching of emission sites, and the creation of defect sites in organic layers. The plasma-induced damage was strongly dependent on the glass transition temperature, exhibiting the most serious degradation in the TAZ with low glass transition temperature.

We have fabricated solution processed organic light-emitting devices (OLEDs) with various hole transporting materials (HTMs) on the plastic substrate. The device structure was ITO/HTM:Ir(2-phq)3 1w...

For efficient and rational utilization of limited bridge maintenance budgets, a method which could be applied to project-level and network-level bridge maintenance decision making issues considerin...

Mega program projects include several sub-projects, require extended periods of time, and incur heavy costs to finish. Because of their project scope, complexity, and size of construction durations...

The new active strengthening system is an excellent system to replace previous external post tensioning systems without causing additional structural problems. In this system, the compressive force...

The Yi Sun-sin Bridge, which is under construction, will be the fourth longest suspension bridge in the world when it is completed, with a main span of 1545 m. The long central span and the...

Existing research concerning construction change order claims deals primarily with system and external problems as the causes of such claims. This study aims at analyzing the attitudes of c...

We investigated hepatoprotective activity and antioxidant effect of the 2,5-dihydroxy-4,3'-di(beta-D-glucopyranosyloxy)-trans-stilbene that purified from Morus bombycis Koidzumi roots against CCl4-induced liver damage in rats. The 2,5-dihydroxy-4,3'-di(beta-D-glucopyranosyloxy)-trans-stilbene displayed dose-dependent superoxide radical scavenging activity (IC50 = 430.2 microg/ml), as assayed by the electron spin resonance (ESR) spin-trapping technique. The increase in aspartate aminotransferase (AST) activities in serum associated with carbon tetrachloride (CCl4)-induced liver injury was inhibited by 2,5-dihydroxy-4,3'-di(beta-D-glucopyranosyloxy)-trans-stilbene and at a dose of 400 - 600 mg/kg samples had hepatoprotective activity comparable to the standard agent, silymarin. The biochemical assays were confirmed by histological observations showing that the 2,5-dihydroxy-4,3'-di(beta-d-glucopyranosyloxy)-trans-stilbene decreased cell ballooning in response to CCl4 treatment. These results demonstrate that the 2,5-dihydroxy-4,3'-di(beta-D-glucopyranosyloxy)-trans-stilbene is a potent antioxidant with a liver protective action against CCl4-induced hepatotoxicity.

To investigate the influence of age on the process of nerve regeneration, the right common peroneal nerves of 14 2 month old and 14 10 month old rats were transected and resutured. At four and eight weeks after the nerve repair, the motor nerve conduction velocity (MNCV), latency, and amplitude of the evoked potential from the peroneus longus muscle were measured. The number of regenerated myelinated fibres, axon diameter, axon area, axon circumference, and myelin thickness were also measured. Compared with the control side (left common peroneal nerve and muscle), MNCV, latency, and amplitude showed higher recovery rates (recovery rate (%) = operated/control x 100) in 2 month old rats than in 10 month old rats, particularly at four weeks after the operation. In the morphometric study, axon diameter, axon area, and myelin thickness also recovered more quickly (recovery rate (%) = operated/control x 100) in 2 month old rats, particularly four weeks after the operation. Morphologically, myelin remnants were not found in 2 month old rats eight weeks after the operation, though they remained in 10 month old rats. These studies show that the recovery rate was significantly greater in 2 month old rats than in 10 month old rats. The explanation seems to be the difference in the speed of Wallerian degeneration, axonal regeneration, and myelin regeneration.