bluuebunny/crossref_metadata_2025_split huggingface dataset:
PflI, a Protein Involved in Flagellar Positioning in
Caulobacter crescentus
Authors: Obuchowski Pamela L. , Jacobs-Wagner Christine 
Published: December 2007

ABSTRACT

The bacterial flagellum is important for motility and adaptation to environmental niches. The sequence of events required for the synthesis of the flagellar apparatus has been extensively studied, yet the events that dictate where the flagellum is placed at the onset of flagellar biosynthesis remain largely unknown. We addressed this question for alphaproteobacteria by using the polarly flagellated alphaproteobacterium
Caulobacter crescentus
as an experimental model system. To identify candidates for a role in flagellar placement, we searched all available alphaproteobacterial genomes for genes of unknown function that cluster with early flagellar genes and that are present in polarly flagellated alphaproteobacteria while being absent in alphaproteobacteria with other flagellation patterns. From this in silico screen, we identified
pflI
. Loss of PflI function in
C. crescentus
results in an abnormally high frequency of cells with a randomly placed flagellum, while other aspects of cell polarization remain normal. In a wild-type background, a fusion of green fluorescent protein (GFP) and PflI localizes to the pole where the flagellum develops. This polar localization is independent of the flagellar protein FliF, whose oligomerization into the MS ring is thought to define the site of flagellar synthesis, suggesting that PflI acts before or independently of this event. Overproduction of PflI-GFP often leads to ectopic localization at the wrong, stalked pole. This is accompanied by a high frequency of flagellum formation at this ectopic site, suggesting that the location of PflI is a sufficient marker for a site for flagellar assembly.
The Type IV Secretion System Component VirB5 Binds to the
trans
-Zeatin Biosynthetic Enzyme Tzs and Enables Its Translocation to the Cell Surface of
Agrobacterium tumefaciens
Authors: Aly Khaled Ahmed , Krall Lilian , Lottspeich Friedrich , Baron Christian 
Published: December 2007

ABSTRACT

VirB5 is a minor component of the extracellular T pilus determined by the
Agrobacterium tumefaciens
type IV secretion system. To identify proteins that interact with VirB5 during the pilus assembly process, we purified VirB5 as a recombinant fusion protein and, by using a gel overlay assay, we detected a 26-kDa interacting protein in
Agrobacterium
cell lysates. The VirB5-binding protein was purified from
A. tumefaciens
and identified as the cytokinin biosynthetic enzyme Tzs. The VirB5-Tzs interaction was confirmed using pulldown assays with purified proteins and the yeast two-hybrid system. An analysis of the subcellular localization in
A. tumefaciens
showed that Tzs was present in the soluble as well as the membrane fraction. Tzs was extracted from the membranes with the mild detergent dodecyl-β-
d
-maltoside in complexes of different molecular masses, and this association was strongly reduced in the absence of VirB5. Using immunoelectron microscopy, we also detected Tzs on the
Agrobacterium
cell surface. A functional type IV secretion system was required for efficient translocation to the surface, but Tzs was not secreted into the cell supernatant. The fact that Tzs localizes on the cell surface suggests that it may contribute to the interaction of
Agrobacterium
with plants.
Nanoarchaeum equitansandIgnicoccus hospitalis: New Insights into a Unique, Intimate Association of Two Archaea
Authors: Jahn Ulrike , Gallenberger Martin , Paper Walter , Junglas Benjamin , Eisenreich Wolfgang , Stetter Karl O. , Rachel Reinhard , Huber Harald 
Published: December 2007

ABSTRACTNanoarchaeum equitansandIgnicoccus hospitalisrepresent a unique, intimate association of two archaea. Both form a stable coculture which is mandatory forN.equitansbut not for the hostI.hospitalis. Here, we investigated interactions and mutual influence between these microorganisms. Fermentation studies revealed that during exponential growth only about 25% ofI.hospitaliscells are occupied byN.equitanscells (one to three cells). The latter strongly proliferate in the stationary phase ofI.hospitalis, until 80 to 90% of theI.hospitaliscells carry around 10N.equitanscells. Furthermore, the expulsion of H2S, the major metabolic end product ofI.hospitalis, by strong gas stripping yields huge amounts of freeN.equitanscells.N.equitanshad no influence on the doubling times, final cell concentrations, and growth temperature, pH, or salt concentration ranges or optima ofI.hospitalis. However, isolation studies using optical tweezers revealed that infection withN.equitansinhibited the proliferation of individualI.hospitaliscells. This inhibition might be caused by deprivation of the host of cell components like amino acids, as demonstrated by13C-labeling studies. The strong dependence ofN.equitansonI.hospitaliswas affirmed by live-dead staining and electron microscopic analyses, which indicated a tight physiological and structural connection between the two microorganisms. No alternative hosts, including otherIgnicoccusspecies, were accepted byN.equitans. In summary, the data show a highly specialized association ofN.equitansandI.hospitaliswhich so far cannot be assigned to a classical symbiosis, commensalism, or parasitism.
Novel Multiplex PCR Assay for Simultaneous Identification of Community-Associated Methicillin-Resistant
Staphylococcus aureus
Strains USA300 and USA400 and Detection of
mecA
and Panton-Valentine Leukocidin Genes, with Discrimination of
Staphylococcus aureus
from Coagulase-Negative Staphylococci
Authors: Zhang Kunyan , McClure Jo-Ann , Elsayed Sameer , Louie Thomas , Conly John M. 
Published: December 2007

ABSTRACT

We developed a novel multiplex PCR assay for rapid identification and discrimination of the USA300 and USA400 strains and concomitant detection of Panton-Valentine leukocidin genes, with simultaneous discrimination of methicillin-resistant
Staphylococcus aureus
strains from methicillin-susceptible
S. aureus
strains,
S. aureus
strains from coagulase-negative staphylococci, and staphylococci from other bacteria.
Comparative Study of Virulence Traits of
Escherichia coli
Clinical Isolates Causing Early and Late Neonatal Sepsis
Authors: Soto S. M. , Bosch J. , Jimenez de Anta M. T. , Vila J. 
Published: December 2007

ABSTRACT

Neonatal meningitis and septicemia caused by
Escherichia coli
are still major health problems in industrialized countries. Forty-seven
E. coli
strains causing neonatal sepsis were analyzed. Twenty-two and 25 strains caused early (detected from 0 to 3 days after birth) and late (detected from 4 to 28 days after birth) infections, respectively. Only the
ibeA
gene was significantly more prevalent in the strains causing early infections.
Contribution of the (1→3)-β-
d
-Glucan Assay for Diagnosis of Invasive Fungal Infections
Authors: Persat Florence , Ranque Stéphane , Derouin Francis , Michel-Nguyen Annie , Picot Stéphane , Sulahian Annie 
Published: December 2007

ABSTRACT

Diagnosis of invasive fungal infection (IFI) remains a challenge. A retrospective study was performed on 279 patients at three French university hospitals to evaluate the performance of the (1→3)-β-
d
-glucan assay (BG assay; Fungitell; Associates of Cape Cod, Inc.) for the diagnosis of IFI. The results of one serum per subject were analyzed for 117 patients who had probable or proven IFI according to the European Organization for Research and Treatment of Cancer criteria (70 invasive pulmonary aspergilloses [IPA], 27 fungal bloodstream infections, and 20
Pneumocystis jiroveci
pneumonias), 40 blood donors, and 122 patients who were hospitalized in hematology wards or intensive care units and were at risk for IFI but in whom IFI had not been diagnosed. For the overall IFI diagnosis, the BG assay had 77.8% sensitivity and specificities of 92.5 and 70.5% for blood donors and patients at risk, respectively. The assay was positive in 48 patients with IPA (68%), in 23 with bloodstream infections (85.2%), and in all who had
P. jiroveci
pneumonias (100%), and the false-positive rate varied depending on the controls used. It allowed a higher rate of detection among IPA patients compared to the galactomannan enzyme-linked immunosorbent assay (ELISA) (48 versus 39 patients, respectively) and among candidemia patients compared to the mannan ELISA (20 versus 11 patients, respectively). This assay therefore appears to be useful in the diagnosis of IFI, particularly for serum analysis of pneumocystosis pneumonia patients, but further studies are needed to evaluate false-positive rates and its future role in IFI diagnosis.
Novel Loop-Mediated Isothermal Amplification Method for Detection of the JP2 Clone of
Aggregatibacter actinomycetemcomitans
in Subgingival Plaque
Authors: Seki Mitsuko , Poulsen Knud , Haubek Dorte , Kilian Mogens 
Published: December 2007

ABSTRACT

We developed a loop-mediated isothermal amplification method that detects the JP2 clone of
Aggregatibacter actinomycetemcomitans
, which induces aggressive periodontitis in adolescents of North and West African descents. Being independent of special equipment, this specific and sensitive method offers significant advantages for screening of patients on a population basis and in clinical settings.
Temporal Association of the Herpes Simplex Virus Genome with Histone Proteins during a Lytic Infection
Authors: Oh Jaewook , Fraser Nigel W. 
Published: December 2007

ABSTRACT
Previous work has determined that there are nucleosomes on the herpes simplex virus (HSV) genome during a lytic infection but that they are not arranged in an equally spaced array like in cellular DNA. However, like in cellular DNA, the promoter regions of several viral genes have been shown to be associated with nucleosomes containing modified histone proteins that are generally found associated with actively transcribed genes. Furthermore, it has been found that the association of modified histones with the HSV genome can be detected at the earliest times postinfection (1 h postinfection) and increases up to 3 h postinfection. However from 3 h to 6 h postinfection (the late phase of the replication cycle), the association decreases. In this study we have examined histone association with promoter regions of all kinetic classes of genes. This was done over the time course of an infection in Sy5y cells using sucrose gradient sedimentation, bromodeoxyuridine labeling, chromatin immunoprecipitation assays, Western blot analysis, trypsin and DNase digestion, and quantitative real-time PCR. Because no histones were detected inside HSV type 1 capsids, the viral genome probably starts to associate with histones after being transported from infecting virions into the host nucleus. Promoter regions of all gene classes (immediate early, early, and late) bind with histone proteins at the start of viral gene expression. However, after viral DNA replication initiates, histones appear not to associate with newly synthesized viral genomes.
Human Immunodeficiency Virus Type 1 Vpr Induces Cell Cycle G
2
Arrest through Srk1/MK2-Mediated Phosphorylation of Cdc25
Authors: Huard Sylvain , Elder Robert T. , Liang Dong , Li Ge , Zhao Richard Y. 
Published: December 2007

ABSTRACT

Human immunodeficiency virus type 1 (HIV-1) Vpr induces cell cycle G
2
arrest in fission yeast (
Schizosaccharomyces pombe
) and mammalian cells, suggesting the cellular pathway(s) targeted by Vpr is conserved among eukaryotes. Our previous studies in fission yeast demonstrated that Vpr induces G
2
arrest in part through inhibition of Cdc25, a Cdc2-specific phosphatase that promotes G
2
/M transition. The goal of this study was to further elucidate molecular mechanism underlying the inhibitory effect of Vpr on Cdc25. We show here that, similar to the DNA checkpoint controls, expression of
vpr
promotes subcellular relocalization of Cdc25 from nuclear to cytoplasm and thereby prevents activation of Cdc2 by Cdc25. Vpr-induced nuclear exclusion of Cdc25 appears to depend on the serine/threonine phosphorylation of Cdc25 and the presence of Rad24/14-3-3 protein, since amino acid substitutions of the nine possible phosphorylation sites of Cdc25 with Ala (9A) or deletion of the
rad24
gene abolished nuclear exclusion induced by Vpr. Interestingly, Vpr is still able to promote Cdc25 nuclear export in mutants defective in the checkpoints (
rad3
and
chk1/cds1
), the kinases that are normally required for Cdc25 phosphorylation and nuclear exclusion of Cdc25, suggesting that others kinase(s) might modulate phosphorylation of Cdc25 for the Vpr-induced G
2
arrest. We report here that this kinase is Srk1. Deletion of the
srk1
gene blocks the nuclear exclusion of Cdc25 caused by Vpr. Overexpression of
srk1
induces cell elongation, an indication of cell cycle G
2
delay, in a similar fashion to Vpr; however, no additive effect of cell elongation was observed when
srk1
and
vpr
were coexpressed, indicating Srk1 and Vpr are likely affecting the cell cycle G
2
/M transition through the same cellular pathway. Immunoprecipitation further shows that Vpr and Srk1 are part of the same protein complex. Consistent with our findings in fission yeast, depletion of the
MK2
gene, a human homologue of Srk1, either by small interfering RNA or an MK2 inhibitor suppresses Vpr-induced cell cycle G
2
arrest in mammalian cells. Collectively, our data suggest that Vpr induces cell cycle G
2
arrest at least in part through a Srk1/MK2-mediated mechanism.
Hepatitis C Virus Core Protein Upregulates Serine Phosphorylation of Insulin Receptor Substrate-1 and Impairs the Downstream Akt/Protein Kinase B Signaling Pathway for Insulin Resistance
Authors: Banerjee Sutapa , Saito Kousuke , Ait-Goughoulte Malika , Meyer Keith , Ray Ratna B. , Ray Ranjit 
Published: December 2007

ABSTRACT

Chronic hepatitis C virus (HCV) infection has a significantly increased prevalence of type 2 diabetes mellitus (T2DM). Insulin resistance is a critical component of T2DM pathogenesis. Several mechanisms are likely to be involved in the pathogenesis of HCV-related insulin resistance. Since we and others have previously observed that HCV core protein activates c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase, we examined the contribution of these pathways to insulin resistance in hepatocytes. Our experimental findings suggest that HCV core protein alone or in the presence of other viral proteins increases Ser
312
phosphorylation of the insulin receptor substrate-1 (IRS-1). Hepatocytes infected with cell culture-grown HCV genotype 1a or 2a displayed a significant increase in the Ser
473
phosphorylation status of the Ser/Thr kinase protein kinase B (Akt/PKB), while Thr
308
phosphorylation was not significantly altered. HCV core protein-mediated Ser
312
phosphorylation of IRS-1 was inhibited by JNK (SP600125) and phosphatidylinositol-3 kinase (LY294002) inhibitors. A functional assay also suggested that hepatocytes expressing HCV core protein alone or infected with cell culture-grown HCV exhibited a suppression of 2-deoxy-
d
-[
3
H]glucose uptake. Inhibition of the JNK signaling pathway significantly restored glucose uptake despite HCV core expression in hepatocytes. Taken together, our results demonstrated that HCV core protein increases IRS-1 phosphorylation at Ser
312
which may contribute in part to the mechanism of insulin resistance.
Genetic Determinants of Sindbis Virus Mosquito Infection Are Associated with a Highly Conserved Alphavirus and Flavivirus Envelope Sequence
Authors: Pierro Dennis J. , Powers Erik L. , Olson Ken E. 
Published: December 2007

ABSTRACT

Wild-type Sindbis virus (SINV) strain MRE16 efficiently infects
Aedes aegypti
midgut epithelial cells (MEC), but laboratory-derived neurovirulent SINV strain TE/5′2J infects MEC poorly. SINV determinants for MEC infection have been localized to the E2 glycoprotein. The E2 amino acid sequences of MRE16 and TE/5′2J differ at 60 residue sites. To identify the genetic determinants of MEC infection of MRE16, the TE/5′2J virus genome was altered to contain either domain chimeras or more focused nucleotide substitutions of MRE16. The growth patterns of derived viruses in cell culture were determined, as were the midgut infection rates (MIR) in
A. aegypti
mosquitoes. The results showed that substitutions of MRE16 E2 aa 95 to 96 and 116 to 119 into the TE/5′2J virus increased MIR both independently and in combination with each other. In addition, a unique PPF/.GDS amino acid motif was located between these two sites that was found to be a highly conserved sequence among alphaviruses and flaviviruses but not other arboviruses.
Replication of ICP0-Null Mutant Herpes Simplex Virus Type 1 Is Restricted by both PML and Sp100
Authors: Everett Roger D. , Parada Carlos , Gripon Philippe , Sirma Hüseyin , Orr Anne 
Published: December 2007

ABSTRACTHerpes simplex virus type 1 (HSV-1) mutants that fail to express the viral immediate-early protein ICP0 have a pronounced defect in viral gene expression and plaque formation in limited-passage human fibroblasts. ICP0 is a RING finger E3 ubiquitin ligase that induces the degradation of several cellular proteins. PML, the organizer of cellular nuclear substructures known as PML nuclear bodies or ND10, is one of the most notable proteins that is targeted by ICP0. Depletion of PML from human fibroblasts increases ICP0-null mutant HSV-1 gene expression, but not to wild-type levels. In this study, we report that depletion of Sp100, another major ND10 protein, results in a similar increase in ICP0-null mutant gene expression and that simultaneous depletion of both proteins complements the mutant virus to a greater degree. Although chromatin assembly and modification undoubtedly play major roles in the regulation of HSV-1 infection, we found that inhibition of histone deacetylase activity with trichostatin A was unable to complement the defect of ICP0-null mutant HSV-1 in either normal or PML-depleted human fibroblasts. These data lend further weight to the hypothesis that ND10 play an important role in the regulation of HSV-1 gene expression.
POISSON–MASLOV TYPE FORMULAS FOR SCHRÖDINGER EQUATIONS WITH MATRIX-VALUED POTENTIALS
Authors: SHAMAROV N. N. 
Published: December 2007

Cauchy problems for Schrödinger equations with matrix-valued potentials are explicitly solved under following assumptions:. — equations are written in momentum form;. — the potentials are Fourier transformed matrix-valued measures with, in general, noncommuting values;. — initial Cauchy data are good enough. The solutions at time t are presented in form of integrals over some spaces of piecewise continuous mappings of the segment [0, t] to a finite-dimensional momentum space, and measures of the integration are countably additive but matrix-valued (resulting in matrices of ordinary Lebesgue integrals). Known results gave solutions either when the measure had commuting (complex) values, or when the integration over infinite dimensional spaces was quite symbolic, or when such integrating was of chronological type and hence more complicated. The method used below is based on technique of matrix-valued transition amplitudes.
Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice
Authors: Tiedt Ralph , Hao-Shen Hui , Sobas Marta A. , Looser Renate , Dirnhofer Stephan , Schwaller Jürg , Skoda Radek C. 
Published: December 2007

Abstract
An acquired somatic mutation in the JAK2 gene (JAK2-V617F) is present in the majority of patients with myeloproliferative disorders (MPDs). Several phenotypic manifestations (polycythemia vera [PV], essential thrombocythemia [ET], and primary myelofibrosis) can be associated with the same mutation. We generated JAK2-V617F transgenic mice using a human JAK2 gene with the sequences encoding the kinase domain placed in the inverse orientation and flanked by antiparallel loxP sites. Crossing mice of one transgenic line (FF1) with transgenic mice expressing Cre-recombinase under the control of the hematopoiesis specific Vav promoter led to expression of JAK2-V617F that was lower than the endogenous wild-type Jak2. These mice developed a phenotype resembling ET with strongly elevated platelet counts and moderate neutrophilia. Induction of the JAK2-V617F transgene with the interferon-inducible MxCre resulted in expression of JAK2-V617F approximately equal to wild-type Jak2 and a PV-like phenotype with increased hemoglobin, thrombocytosis, and neutrophilia. Higher levels of JAK2-V617F in mouse bone marrow by retroviral transduction caused a PV-like phenotype without thrombocytosis. These data are consistent with the hypothesis that the ratio of mutant to wild-type JAK2 is critical for the phenotypic manifestation. A similar correlation was also found in patients with MPD.
Cooperative signaling through the signal transducer and activator of transcription 3 and nuclear factor-κB pathways in subtypes of diffuse large B-cell lymphoma
Authors: Lam Lloyd T. , Wright George , Davis R. Eric , Lenz Georg , Farinha Pedro , Dang Lenny , Chan John W. , Rosenwald Andreas , Gascoyne Randy D. , Staudt Louis M. 
Published: December 2007

AbstractThe activated B cell–like (ABC) subgroup of diffuse large B-cell lymphoma (DLBCL) is characterized by constitutive activation of the nuclear factor-κB (NF-κB) pathway. In this study, we showed that the NF-κB pathway induced the expression of the cytokines interleukin (IL)-6 and IL-10 in ABC DLBCL cell lines, which also have high levels of total and phosphorylated signal transducer and activator of transcription (STAT) 3 protein, suggesting autocrine signaling. Using RNA interference for STAT3, we defined a gene expression signature of IL-6 and IL-10 signaling through STAT3. Based on this signature, we constructed a molecular predictor of STAT3 signaling that defined a subset of ABC DLBCL tumors with high expression of STAT3, IL-6, and/or IL-10 and their downstream targets. Although the STAT3-high and STAT3-low subsets had equivalent expression of genes that distinguish ABC DLBCL from germinal center B cell–like DLBCL, STAT3-high ABC DLBCLs had higher expression of signatures that reflected NF-κB activity, proliferation, and glycolysis. A small-molecule inhibitor of Janus kinase signaling, which blocked STAT3 signature expression, was toxic only for ABC DLBCL lines and synergized with an inhibitor of NF-κB signaling. These findings suggest that the biological interplay between the STAT3 and NF-κB pathways may be exploited for the treatments of a subset of ABC DLBCLs.
Occult connective tissue diseases mimicking idiopathic interstitial pneumonias
Authors: Tzelepis G. E. , Toya S. P. , Moutsopoulos H. M. 
Published: December 2007

In patients with interstitial lung disease (ILD), the diagnosis of idiopathic interstitial pneumonia is usually made after excluding, among other conditions, connective tissue diseases (CTDs). Although in most patients with a CTD and respiratory symptoms, the systemic nature of the disease is obvious, the ILD-related manifestations in CTDs may often dominate the clinical picture or precede systemic findings and thus mimic idiopathic interstitial pneumonia.With the exception of systemic lupus erythematosus, all CTDs may imitate chronic idiopathic interstitial pneumonias. In this setting, clues to an underlying CTD may be entirely absent or include subtle findings from various systems, including skin, vascular and musculoskeletal system or internal organs. Since nonspecific interstitial pneumonia is a relatively frequent histological pattern in CTDs, biopsy reports of nonspecific interstitial pneumonia should also prompt a search for an underlying CTD.Ultimately, diagnosis of a CTD requires confirmation with immunological testing; interpretation of the various laboratory tests should always be carried out in conjunction with clinical findings.The present article reviews specific clinical aspects of connective tissue disease-related interstitial lung disease that may help differentiate it from idiopathic interstitial pneumonia, especially when interstitial lung disease is the predominant or sole manifestation of an occult connective tissue disease.