10 results match your criteria: "and Seattle Biomedical Research Institute[Affiliation]"

Chronic HIV-1 Infection Impairs Superantigen-Induced Activation of Peripheral CD4+CXCR5+PD-1+ Cells, With Relative Preservation of Recall Antigen-Specific Responses.

J Acquir Immune Defic Syndr

January 2017

*Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN; †Flow Cytometry Shared Resource, Vanderbilt University Medical Center, Nashville, TN; ‡Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN; and §Seattle Biomedical Research Institute, Seattle, WA.

Peripheral CD4+CXCR5+PD-1+ T cells are a putative circulating counterpart to germinal center T follicular helper (TFH) cells. They show both phenotypic and functional similarities to TFH cells, which provide necessary help for the differentiation of B cells to antibody-secreting plasmablasts. In this study, we evaluated the frequency, phenotypes, and responses of peripheral TFH-like (pTFH) cells to superantigen and recall antigen stimulation in 10 healthy and 34 chronically infected treatment-naive HIV-1+ individuals.

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Bacteremia and malaria in Tanzanian children hospitalized for acute febrile illness.

J Trop Pediatr

April 2015

Laboratory of Malaria Immunology and Vaccinology, NIAID, Bethesda, MD, USA.

We recorded the reason for presentation to a rural hospital in an area endemic for malaria in 909 children between January 2006 and March 2009. Blood smears were examined for Plasmodium falciparum parasites, and blood spots dried on filter paper were prepared for 464 children. A PCR assay utilizing the stored blood spots was developed for Streptococcus pneumoniae (lytA) and Haemophilus influenzae (pal).

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PhosphoChain: a novel algorithm to predict kinase and phosphatase networks from high-throughput expression data.

Bioinformatics

October 2013

Institute for Systems Biology, Seattle, WA 98109-5234, USA, Department of Computer Science and Information Engineering, National Cheng Kung University, Tainan, Taiwan and Seattle Biomedical Research Institute, Seattle, WA 98109-5219, USA.

Motivation: Protein phosphorylation is critical for regulating cellular activities by controlling protein activities, localization and turnover, and by transmitting information within cells through signaling networks. However, predictions of protein phosphorylation and signaling networks remain a significant challenge, lagging behind predictions of transcriptional regulatory networks into which they often feed.

Results: We developed PhosphoChain to predict kinases, phosphatases and chains of phosphorylation events in signaling networks by combining mRNA expression levels of regulators and targets with a motif detection algorithm and optional prior information.

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Exchange of macromolecules between the nucleus and cytoplasm is a key regulatory event in the expression of a cell's genome. This exchange requires a dedicated transport system: (1) nuclear pore complexes (NPCs), embedded in the nuclear envelope and composed of proteins termed nucleoporins (or "Nups"), and (2) nuclear transport factors that recognize the cargoes to be transported and ferry them across the NPCs. This transport is regulated at multiple levels, and the NPC itself also plays a key regulatory role in gene expression by influencing nuclear architecture and acting as a point of control for various nuclear processes.

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Caspofungin (CSP) susceptibilities of Candida albicans, as determined by broth microdilution methods, have not been found to be related to azole susceptibilities or resistance. In contrast, it has been observed that azole-resistant clinical isolates that overexpress the efflux pump gene CDR2 are less susceptible to CSP when tested using an agar dilution method commonly employed with Saccharomyces cerevisiae. The goal of this study was to further understand the effects of azole resistance mechanisms on CSP susceptibility testing.

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cis-Acting elements within the Candida albicans ERG11 promoter mediate the azole response through transcription factor Upc2p.

Eukaryot Cell

December 2007

Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, and Seattle Biomedical Research Institute, Seattle, Washington 98109-5219, USA.

The azole antifungal drugs are used to treat infections caused by Candida albicans and other fungi. These drugs interfere with the biosynthesis of ergosterol, the major sterol in fungal cells, by inhibiting an ergosterol biosynthetic enzyme, lanosterol 14 alpha-demethylase, encoded by the ERG11 gene. In vitro, these drugs as well as other ergosterol biosynthesis inhibitors increase ERG11 mRNA expression by activation of the ERG11 promoter.

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The Candida albicans lanosterol 14-alpha-demethylase (ERG11) gene promoter is maximally induced after prolonged growth with antifungal drugs.

Antimicrob Agents Chemother

April 2004

Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, and Seattle Biomedical Research Institute, Seattle, Washington 98109, USA.

The azole antifungal drugs that target lanosterol 14-alpha-demethylase, encoded by the ERG11 gene, are used to treat a variety of infections caused by Candida albicans. Azoles are known to induce expression of ERG11 mRNA. The ERG11 promoter was cloned 5' of the luciferase-coding region, and the induction of ERG11 expression by azoles was monitored by luciferase assays.

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The composition of the editosome, a multi-protein complex that catalyzes uridine insertion and deletion RNA editing to produce mature mitochondrial mRNAs in trypanosomes, was analyzed by mass spectrometry. The editosomes were isolated by column chromatography, glycerol gradient sedimentation, and monoclonal antibody affinity purifications. At least 16 proteins form the catalytic core of the editosome, and additional associated proteins were identified.

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The presence of an R467K amino acid substitution and loss of allelic variation correlate with an azole-resistant lanosterol 14alpha demethylase in Candida albicans.

Antimicrob Agents Chemother

July 1997

Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, and Seattle Biomedical Research Institute, 98109, USA.

Azole resistance in the pathogenic yeast Candida albicans is an emerging problem in the human immunodeficiency virus (HIV)-infected population. The target enzyme of the azole drugs is lanosterol 14alpha demethylase (Erg16p), a cytochrome P-450 enzyme in the biosynthetic pathway of ergosterol. Biochemical analysis demonstrates that Erg16p became less susceptible to fluconazole in isolate 13 in a series of isolates from an HIV-infected patient.

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Increased mRNA levels of ERG16, CDR, and MDR1 correlate with increases in azole resistance in Candida albicans isolates from a patient infected with human immunodeficiency virus.

Antimicrob Agents Chemother

July 1997

Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, and Seattle Biomedical Research Institute, 98109, USA.

Resistance to antifungal drugs, specifically azoles such as fluconazole, in the opportunistic yeast Candida albicans has become an increasing problem in human immunodeficiency virus (HIV)-infected individuals. The molecular mechanisms responsible for this resistance have only recently become apparent and can include alterations in the target enzyme of the azole drugs (lanosterol 14alpha demethylase [14DM]), or in various efflux pumps from both the ABC transporter and major facilitator gene families. To determine which of these possible mechanisms was associated with the development of drug resistance in a particular case, mRNA levels have been studied in a series of 17 clinical isolates taken from a single HIV-infected patient over 2 years, during which time the levels of fluconazole resistance of the strain increased over 200-fold.

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