bluuebunny/crossref_metadata_2025_split huggingface dataset:
Latent Protein LANA2 from Kaposi's Sarcoma-Associated Herpesvirus Interacts with 14-3-3 Proteins and Inhibits FOXO3a Transcription Factor
Authors: Muñoz-Fontela Cesar , Marcos-Villar Laura , Gallego Pedro , Arroyo Javier , Da Costa Marco , Pomeranz Karen M. , Lam Eric W.-F. , Rivas Carmen 
Published: November 2006

ABSTRACT

The Kaposi's sarcoma-associated herpesvirus latent protein LANA2 has been suggested to have an important role in the transforming activity of the virus based on its capacity to inhibit p53 and PKR-dependent apoptosis as well as the interferon-dependent response. Here, we describe a novel interaction between LANA2 and both the phosphoserine/phosphothreonine-binding 14-3-3 proteins and the transcription factor FOXO3a. In addition, our results indicate that LANA2 inhibits the transcriptional activity of FOXO3a and blocks the G
2
/M arrest induced by 14-3-3 protein overexpression. These results suggest a novel mechanism by which LANA2 may promote tumorigenesis.
Preferential Activation of Toll-Like Receptor Nine by CD46-Utilizing Adenoviruses
Authors: Iacobelli-Martinez Milena , Nemerow Glen R. 
Published: November 2006

ABSTRACT
Adenoviruses (Ads) are responsible for respiratory, ocular, and gastrointestinal illnesses in humans. While the majority of serotypes utilize coxsackievirus-adenovirus receptor (CAR) as their primary attachment receptor, subgroup B and subgroup D Ad37 serotypes use CD46. Given the propensity of Ad vectors to activate host immune responses, we sought to investigate their potential for type I interferon induction. We found that CD46 Ads were capable of alpha interferon (IFN-α) induction by peripheral blood mononuclear cells and that plasmacytoid dendritic cells (pDCs) were the principal producers of this cytokine. IFN-α induction correlated with the permissivity of pDCs to CD46- but not CAR-utilizing Ad serotypes. A role for Toll-like receptor 9 (TLR9) recognition of Ad was supported by the requirement for viral DNA and efficient endosomal acidification and by the ability of a TLR9-inhibitory oligonucleotide to attenuate IFN-α induction. Cell lines expressing TLR9 that are permissive to infection by both CAR- and CD46-utilizing serotypes showed a preferential induction of TLR9-mediated events by CD46-utilizing Ads. Specifically, the latter virus types induced higher levels of cytokine expression and NF-κB activation in HeLa cells than CAR-dependent Ad types, despite equivalent infection rates. Therefore, infectivity alone is not sufficient for TLR9 activation, but this activation instead is regulated by a specific receptor entry pathway. These data reveal a novel mode of host immune recognition of Ad with implications for Ad pathogenesis and for the use of unconventional Ad vectors for gene delivery and vaccine development.
CXCR3-Dependent Recruitment of Antigen-Specific T Lymphocytes to the Liver during Murine Cytomegalovirus Infection
Authors: Hokeness Kirsten L. , Deweerd Elizabeth S. , Munks Michael W. , Lewis Casey A. , Gladue Ronald P. , Salazar-Mather Thais P. 
Published: November 2006

ABSTRACTInnate inflammatory events promoting antiviral defense in the liver against murine cytomegalovirus (MCMV) infection have been characterized. However, the mechanisms that regulate the selective recruitment of inflammatory T lymphocytes to the liver during MCMV infection have not been defined. The studies presented here demonstrate the expression of monokine induced by gamma interferon (IFN-γ; Mig/CXCL9) and IFN-γ-inducible protein 10 (IP-10/CXCL10) in liver leukocytes and correlate their production with the infiltration of MCMV-specific CD8 T cells into the liver. Antibody-mediated neutralization of CXCL9 and CXCL10 and studies using mice deficient in CXCR3, the primary known receptor for these chemokines, revealed that CXCR3-dependent mechanisms promote the infiltration of virus-specific CD8 T cells into the liver during acute infection with MCMV. Furthermore, CXCR3 functions augmented the hepatic accumulation of CD8 T-cell IFN-γ responses to MCMV. Evaluation of protective functions demonstrated enhanced pathology that overlapped with transient increases in virus titers in CXCR3-deficient mice. However, ultimate viral clearance and survival were not compromised. Thus, CXCR3-mediated signals support the accumulation of MCMV-specific CD8 T cells that contribute to, but are not exclusively required for, protective responses in a virus-infected tissue site.
Increased muscle oxidative potential following resistance training induced fibre hypertrophy in young men
Authors: Tang Jason E. , Hartman Joseph W. , Phillips Stuart M. 
Published: November 2006

Some evidence suggests that resistance training may lower relative muscle mitochondrial content via “dilution” of the organelle in a larger muscle fibre. Such an adaptation would reduce fatigue resistance, as well as compromise oxidative ATP synthesis and the capacity for fatty-acid oxidation. We investigated the effect of resistance training on mitochondrial enzymes of the citric acid cycle (citrate synthase; CS) and β-oxidation (β-hydroxyacyl CoA dehydrogenase; β-HAD), as well as markers of the potential for glucose phosphorylation (hexokinase; HK) and glycolysis (phosphofructokinase; PFK). Twelve untrained men (21.9 ± 0.5 y; 1.79 ± 0.03 m; 83.2 ± 3.2 kg) participated in a 12 week progressive resistance-training program. Muscle biopsies were taken from the vastus lateralis before (PRE) and after (POST) training. Training increased mean muscle fibre cross-sectional area (p < 0.05) and the activities of CS (PRE = 4.53 ± 0.44 mol·kg protein–1·h–1; POST = 5.63 ± 0.40 mol·kg protein–1·h–1; p < 0.001) and β-HAD (PRE = 2.55 ± 0.28 mol·kg protein–1·h–1; POST = 3.11 ± 0.21 mol·kg protein–1·h–1; p < 0.05). The activity of HK increased 42% (p < 0.05), whereas the activity of PFK remained unchanged. We conclude that resistance training provides a stimulus for improving muscle oxidative potential, as reflected by the increased activities of CS and β-HAD following resistance training induced hypertrophy.
Mutant p53 Protects Cells from 12-O-Tetradecanoylphorbol-13-Acetate–Induced Death by Attenuating Activating Transcription Factor 3 Induction
Authors: Buganim Yosef , Kalo Eyal , Brosh Ran , Besserglick Hila , Nachmany Ido , Rais Yoach , Stambolsky Perry , Tang Xiaohu , Milyavsky Michael , Shats Igor , Kalis Marina , Goldfinger Naomi , Rotter Varda 
Published: November 2006

Abstract
Mutations in p53 are ubiquitous in human tumors. Some p53 mutations not only result in loss of wild-type (WT) activity but also grant additional functions, termed “gain of function.” In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway. We show that high doses of TPA induce ATF3 in a WT p53-independent manner correlating with PKCs depletion and cell death. We show that cells harboring mutant p53 have attenuated ATF3 induction and are less sensitive to TPA-induced death compared with their p53-null counterparts. Mutagenesis analysis of the ATF3 promoter identified the regulatory motifs cyclic AMP-responsive element binding protein/ATF and MEF2 as being responsible for the TPA-induced activation of ATF3. Moreover, we show that mutant p53 attenuates ATF3 expression by two complementary mechanisms. It interacts with the ATF3 promoter and influences its activity via the MEF2 site, and additionally, it attenuates transcriptional expression of the ATF3 activator MEF2D. These data provide important insights into the molecular mechanisms that underlie mutant p53 gain of function. (Cancer Res 2006; 66(22): 1750-9)
Oxidative Stress Induces Premature Senescence by Stimulating Caveolin-1 Gene Transcription through p38 Mitogen-Activated Protein Kinase/Sp1–Mediated Activation of Two GC-Rich Promoter Elements
Authors: Dasari Arvind , Bartholomew Janine N. , Volonte Daniela , Galbiati Ferruccio 
Published: November 2006

Abstract
Cellular senescence is believed to represent a natural tumor suppressor mechanism. We have previously shown that up-regulation of caveolin-1 was required for oxidative stress–induced premature senescence in fibroblasts. However, the molecular mechanisms underlying caveolin-1 up-regulation in senescent cells remain unknown. Here, we show that subcytotoxic oxidative stress generated by hydrogen peroxide application promotes premature senescence and stimulates the activity of a (−1,296) caveolin-1 promoter reporter gene construct in fibroblasts. Functional deletion analysis mapped the oxidative stress response elements of the mouse caveolin-1 promoter to the sequences −244/−222 and −124/−101. The hydrogen peroxide–mediated activation of both Cav-1 (−244/−222) and Cav-1 (−124/−101) was prevented by the antioxidant quercetin. Combination of electrophoretic mobility shift studies, chromatin immunoprecipitation analysis, Sp1 overexpression experiments, as well as promoter mutagenesis identifies enhanced Sp1 binding to two GC-boxes at −238/−231 and −118/−106 as the core mechanism of oxidative stress–triggered caveolin-1 transactivation. In addition, signaling studies show p38 mitogen-activated protein kinase (MAPK) as the upstream regulator of Sp1-mediated activation of the caveolin-1 promoter following oxidative stress. Inhibition of p38 MAPK prevents the oxidant-induced Sp1-mediated up-regulation of caveolin-1 protein expression and development of premature senescence. Finally, we show that oxidative stress induces p38-mediated up-regulation of caveolin-1 and premature senescence in normal human mammary epithelial cells but not in MCF-7 breast cancer cells, which do not express caveolin-1 and undergo apoptosis. This study delineates for the first time the molecular mechanisms that modulate caveolin-1 gene transcription upon oxidative stress and brings new insights into the redox control of cellular senescence in both normal and cancer cells. (Cancer Res 2006; 66(22): 10805-14)
Up-regulation of Heat Shock Protein 27 Induces Resistance to 17-Allylamino-Demethoxygeldanamycin through a Glutathione-Mediated Mechanism
Authors: McCollum Andrea K. , TenEyck Cynthia J. , Sauer Brian M. , Toft David O. , Erlichman Charles 
Published: November 2006

Abstract
17-Allylamino-demethoxygeldanamycin (17-AAG), currently in phase I and II clinical trials as an anticancer agent, binds to the ATP pocket of heat shock protein (Hsp90). This binding induces a cellular stress response that up-regulates many proteins including Hsp27, a member of the small heat shock protein family that has cytoprotective roles, including chaperoning of cellular proteins, regulation of apoptotic signaling, and modulation of oxidative stress. Therefore, we hypothesized that Hsp27 expression may affect cancer cell sensitivity to 17-AAG. In colony-forming assays, overexpression of Hsp27 increased cell resistance to 17-AAG whereas down-regulation of Hsp27 by siRNA increased sensitivity. Because Hsp27 is known to modulate levels of glutathione (GSH), we examined cellular levels of GSH and found that it was decreased in cells transfected with Hsp27 siRNA when compared with control siRNA. Treatment with buthionine sulfoximine, an inhibitor of GSH synthesis, also sensitized cells to 17-AAG. Conversely, treatment of Hsp27 siRNA–transfected cells with N-acetylcysteine, an antioxidant and GSH precursor, reversed their sensitivity to 17-AAG. A cell line selected for stable resistance to geldanamycin relative to parent cells showed increased Hsp27 expression. When these geldanamycin- and 17-AAG-resistant cells were transfected with Hsp27 siRNA, 17-AAG resistance was dramatically diminished. Our results suggest that Hsp27 up-regulation has a significant role in 17-AAG resistance, which may be mediated in part through GSH regulation. Clinical modulation of GSH may therefore enhance the efficacy of Hsp90-directed therapy. (Cancer Res 2006; 66(22): 10967-75)
Infrared study of goethites of varying crystallinity and particle size: I. Interpretation of OH and lattice vibration frequencies
Authors: Cambier P. 
Published: November 2006

AbstractA detailed study of the IR spectrum of goethite is given with the aim of relating variations to crystalline order and particle size. The OH stretching vibrations are split into two active components at high frequency, plus two inactive ones at low frequency. Two different bending modes exist from site group splitting. Their active modes from factor group splitting are at lower frequencies than the uncoupled ones. The lattice bands at 630 and 400 cm−1 correspond to Fe-O or Fe-OH stretching, approximately parallel to a and c, and thus respectively sensitive and not sensitive to the particle shape, as long as it remains elongated along c.
Diagenetic carbonate and evaporite minerals in Rotliegend aeolian sandstones of the Southern North Sea: their nature and relationship to secondary porosity development
Authors: Pye K. , Krinsley D. H. 
Published: November 2006

AbstractDeeply buried (> 3·5 km) Rotliegend aeolian sandstones in the Southern North Sea Basin display a number of interesting diagenetic features including (i) zoned iron-rich carbonate cements, (ii) anhydrite, halite and baryte cements, (iii) at least two generations of authigenic illite, and (iv) significant secondary porosity created by cement and framework-grain dissolution. The creation and destruction of secondary porosity is the result of changes in porewater chemistry during burial and subsequent uplift. Three pore-fluid regimes can be identified: (1) alkaline, oxidizing conditions during shallow to intermediate burial; (2) acid, reducing conditions during intermediate to deep burial; (3) alkaline, reducing conditions during deep burial and uplift. The transition from stage 1 to stage 2 was probably caused by expulsion of waters from the underlying Carboniferous shales. The transition to stage 3 probably began when faulting associated with uplift allowed invasion by alkaline fluids derived from Zechstein sediments.
Diagenesis of the shallow marine Fulmar Formation in the Central North Sea
Authors: Stewart D. J. 
Published: November 2006

AbstractThe diagenetic history of the Upper Jurassic Fulmar Formation of the Central North Sea is described with emphasis on the Fulmar Field. The Fulmar Formation was deposited on a variably subsiding shallow-marine shelf under the influence of halokinetic and fault movements. The sediments are extensively bio-destratified although large-scale cross-bedding is locally preserved. The dominant mechanism of deposition is thought to have been storm-generated currents. Soft-sediment deformation structures are common and are attributed to syn- and post-depositional dewatering of the sandstones. The dewatering was associated with fractures and shear zones which reflect tectonic instability resulting from periodic salt withdrawal and/or graben fault movements. The dewatering may have been initiated by repacking of the sediments during earth movements or by the gradual build-up and sudden release of overpressures due to compaction and/or clay mineral dehydration during rapid burial at the end of the Cretaceous. The formation is composed of arkosic sandstone of similar composition to Triassic sandstones from which it was probably derived. The sandstones also contain limited amounts of marine biogenic debris including sponge solenasters, bivalve shells, rare ammonites and belemnites. Initial diagenesis began with an environment-related phase during which quartz and feldspar overgrowths and chalcedony and calcite cements were precipitated. These cements appear to form concretions adjacent to local concentrations of sponge debris and shell debris, respectively, and were disturbed after their formation by fracturing and dewatering. This was followed by an early burial stage of diagenesis which resulted in extensive dolomite cementation and minor clay mineral authigenesis (illite and chlorite). The last phase of mineral growth was probably pyrite. During early burial diagenesis, secondary porosity after feldspar and/or carbonate was produced, although the exact timing is not clear. The lack of both stylolitic developments and extensive illitization indicates that the late burial diagenesis stage was never reached, although sufficient clay diagenesis occurred to destroy all traces of mixed-layer illite-smectite (present in some shallower wells). The main control on reservoir behaviour is primary depositional fabric. Diagenesis only overprints these controls. Locally-cemented fracture sets act as baffles to fluid flow, but they are not extensive and the reservoir acts as one unit.
An SEM study of phyllosilicate diagenesis in sandstones and mudstones in the Westphalian Coal Measures using back-scattered electron microscopy
Authors: Huggett J. M. 
Published: November 2006

AbstractBack-scattered electron imaging was used in conjunction with energy-dispersive spectral analysis to study phyllosilicate minerals in polished thin-sections of Carboniferous (Westphalian) sandstones and associated mudstones from the East Midlands and from the diagenetically higher grade area of Abernant in the South Wales coalfield. Chemical diagenesis proceeded more rapidly in the sandstones than in the mudstones. In the East Midlands, greater flow of freshwater through the sandstones than the mudstones produced a higher degree of alteration of muscovite to kaolinite in the sandstones. Chlorite is present in the Well 1 and Well 2 East Midlands sandstones but not the mudstones nor any Well 3 samples. The chlorite may be an early diagenetic replacement of biotite. Much chlorite has been replaced by kaolinite. In the Abernant samples chlorite is present in both the sandstones and mudstones. In the former it appears to have replaced detrital biotite. In the latter the chlorite is too fine-grained to discern whether it is detrital or authigenic. The chlorite may have formed during the Hercynian orogeny. Much of the mica and chlorite in the Abernant sandstones has been replaced by illite, possibly in the post-orogenic period. The scarcity of kaolinite in the Abernant samples reflects the lack of freshwater leaching.
Sandstone reservoir description: an overview of the role of geology and mineralogy
Authors: Hurst A. , Archer J. S. 
Published: November 2006

AbstractReservoir description is achieved by the integration of geological, petrophysical and engineering data. Modelling of reservoir performance is made by creating a three-dimensional model of the reservoir volume, where the reservoir is built of cells and layered zones which are defined geologically. Although the scale of cell size is coarse compared to the scale of geological data, it is important that the geological input to define cells is as precise as possible. The texture of clay minerals and their composition are requisite for understanding their influence on reservoir characteristics. Wireline logs probably do not provide sufficient information about clay mineralogy to evaluate reservoir characteristics, but do allow the extrapolation of ‘point’ mineralogical data into a continuous reservoir description. Evaluation of porosity, permeability and saturation are described, and the possible influence of clay mineralogy on evaluation of these characteristics is discussed.
Moisture damage and childhood asthma: a population-based incident case–control study
Authors: Pekkanen J. , Hyvärinen A. , Haverinen-Shaughnessy U. , Korppi M. , Putus T. , Nevalainen A. 
Published: November 2006

Most previous studies on the association between moisture damage and asthma have been cross-sectional and relied on self-reported exposure and health. The present authors studied the association by carrying out careful home inspections among new, clinically determined cases of asthma and controls.New cases of asthma aged 12–84 months (n = 121) were recruited prospectively and matched for year of birth, sex and living area with two randomly selected population controls (n = 241). Trained engineers visited all homes. Both cases and controls had lived ≥75% of their lifetime or the past 2 yrs in their current home.Risk of asthma increased with severity of moisture damage and presence of visible mould in the main living quarters but not in other areas of the house. Cases more often had damage in their bedroom. Associations were comparable for atopic and nonatopic asthma and for children aged >30 months or ≤30 months.The present results, using standardised assessment of exposure and asthma, suggest that moisture damage and mould growth in the main living quarters are associated with the development of asthma in early childhood.
Prediction of cloth wetting times from diffusion constants of alcohol ethoxylate mixtures
Authors: Smith Dewey L. 
Published: November 2006

AbstractCommercial alcohol ethoxylates are composed of a distribution of ethoxymers, and the width of the distribution can affect some performance properties such as cloth wetting. For example, if the distribution is peaked at the fastest wetting ethoxymer, wetting time decreases. One can predict if further peaking will significantly improve wetting performance if the relationship between ethoxymer distribution peaking and wetting can be determined. As a first step in predicting how cloth wetting time changes with peaking of the ethoxymer distribution, the cloth wetting time of a binary mixture of octaethylene glycol monododecyl ether (C12−8) and hexaethylene glycol monotetradecyl ether (C14−6) was studied. Wetting time was inversely dependent on the average diffusion constant of the mixture, which is predicted from the diffusion constants of the ethoxymers in the mixture and the mixture composition. Diffusion constants of the ethoxymers are derived from dynamic surface tension measurements. Therefore, it is possible to predict the relative cloth wetting time for any alcohol ethoxylate distribution by knowing the diffusion constant of each ethoxymer in the distribution and the distribution composition.
Conductance behavior of lithium soaps in aqueous methanol
Authors: Varma R. P. , Goel H. 
Published: November 2006

AbstractConductance behavior of lithium soaps (abietate, oleate, and myristate) has been used to evaluate the true dissociation constant, limiting molar conductance, and thermodynamic parameters (viz., enthalpy, free energy, and entropy changes) for dissociation. The soaps behave as week electrolytes in mixtures, and the Debye‐Huckel‐Onsagar equation is not applicable for these soap solutions.
Use of certain alcohol ethoxylates to maintain protease stability in the presence of anionic surfactants
Authors: Russell Geoffrey L. , Britton Larry N. 
Published: November 2006

AbstractAnionic surfactants, including linear alkylbenzene sulfonate (LAS), are known to decrease the stability of detergent proteases, possibly by hastening autoproteolytic processes. Thus, protease shelf life in enzyme‐containing, heavy‐duty liquid laundry detergents (HDL) is typically maintained by adding stabilizers, by limiting the level of interfering anionics, or by utilizing more compatible anionics, such as alcohol ethoxysulfates (AES). This study examines the stability of Savinase® detergent protease in HDL formulations based on LAS and containing different alcohol ethoxylates (AE) for protection against protease inactivation. Dose response curves demonstrated that all commonly used anionic surfactants except AES promote loss of protease activity. In HDL formulations with equal percentage compositions of LAS and AE, the structure of the selected AE was found to have a profound influence on protease stability. Inclusion of AE with chain length ≥C14 and ethoxylate levels >70% resulted in greater protease stability. HDL containing LAS and these protective AE could be formulated to achieve protease stability matching those of simulated commercial products. Unlike polyhydric stabilizers, the AE by themselves confer no additional stability to the protease. It is more likely that the stabilizing effect of the “protective” AE is due to decreased availability of LAS to the protease.