1,733,545 research outputs found
Child background characteristics (N = 1291).
No full textChild background characteristics (N = 1291).</p
Campylobacter jejuni 1291 in cell morphology and pathogenesis
No full textCampylobacter jejuni is a widespread enteric pathogen that causes mild to severe gastroenteritis in humans. Despite the prevalence of C. jejuni, its virulence mechanisms are poorly understood. It had long been postulated that C. jejuni’s characteristic helical shape was important for pathogenesis, which our group has now shown to be the case. Peptidoglycan remodelling enzymes play a key role in maintaining cell shape. The LytM domain-containing protein 1291 was identified while searching the C. jejuni genome for peptidoglycan peptidases. As 1291 was predicted to lack proteolytic activity, it was subsequently predicted to activate the C. jejuni amidase, AmiA. Deletion of 1291 caused distinct phenotypic changes compared to wild type C. jejuni. The 1291 deletion mutant demonstrated a long chain-like cellular morphology similar to an amiA deletion strain and contributed to key pathogenesis phenotypes. In comparison to wild type, ∆1291 displayed severe motility and autoagglutination defects, as well as an increase in biofilm formation. Both 1291 and the E. coli LytM domain-containing amidase activator EnvC showed cross-species complementation. Specifically, 1291 was able to complement the severe chaining phenotype of an E. coli amidase activator deletion strain, and EnvC was able to complement the chain-like phenotype of ∆1291. This work provides evidence that 1291 acts as a pathogenesis factor in C. jejuni and is involved in cellular morphological changes, likely through the activation of C. jejuni’s sole amidase, AmiA.Science, Faculty ofMicrobiology and Immunology, Department ofGraduat
Impact and mechanistic role of MicroRNA-1291 on pancreatic tumorigenesis.
No full text 243 Background: Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer death. Better understanding of pancreatic cancer biology and identification of new targets are highly warranted. MicroRNAs (miRs or miRNAs) play a critical role in the control of tumor progression via crosstalk with cancer signaling pathways. Our recent studies showed that miR-1291 improved chemosensitivity through targeting of efflux transporter ABCC1. This current study investigated the mechanistic role of miR-1291 in the suppression of pancreatic tumorigenesis. Methods: PANC-1 and AsPC-1 cell lines were stably transfected with miR-1291. Cell cycle status and apoptosis of stable miR-1291-expressing cells were tested against control cells using flow cytometry. Cells were injected subcutaneously into nude mice and tumorigenesis was measured in vivo. Proteomic studies were performed by two-dimensional difference gel electrophoresis, matrix-assisted laser desorption/ionization time of flight mass spectrometry analysis. Computationally predicted miR-1291 targets were assessed by luciferase reporter assay and Western blot. Primary PDAC and control samples were tested for miR-1291 and target gene expression levels. Results: Our data showed that stable miR-1291-expressing PANC-1 and AsPC-1 cells both showed a significantly lower rate of proliferation than the control cells, which was associated with a cell cycle arrest and enhanced apoptosis. Furthermore, miR-1291 suppressed the tumorigenesis of PANC-1 cells in mouse models in vivo. Proteomic studies revealed the protein level of several cancer-related genes were downregulated by miR-1291, including a pancreatic tumor promoting protein AGR2 which was reduced ~10-fold. Through computational and experimental studies we further identified that FOXA2, a transcription factor governing AGR2 expression, was a direct target of miR-1291. In addition, we found a significant down-regulation of miR-1291 in a set of PDAC patient tumor samples overexpressing AGR2. Conclusions: These results indicate that miR-1291 suppresses pancreatic tumorigenesis via targeting of FOXA2-AGR regulatory pathway providing new insight supporting development of miR-1291-based therapy for PDAC. </jats:p
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Background characteristics of the mother (N = 1291).
No full textBackground characteristics of the mother (N = 1291).</p
MicroRNA-1291-mediated silencing of IRE1 enhances Glypican-3 expression
No full textInternational audienceMicroRNAs (miRNA) are generally described as negative regulators of gene expression. However, some evidence suggests that they may also play positive roles. As such, we reported that miR-1291 leads to a GPC3 mRNA expression increase in hepatoma cells through a 3' untranslated region (UTR)-dependent mechanism. In the absence of any direct interaction between miR-1291 and GPC3 mRNA, we hypothesized that miR-1291 could act by silencing a negative regulator of GPC3 mRNA expression. Based on in silico predictions and experimental validation, we demonstrate herein that miR-1291 represses the expression of the mRNA encoding the endoplasmic reticulum (ER)-resident stress sensor IRE1α by interacting with a specific site located in the 5' UTR. Moreover, we show, in vitro and in cultured cells, that IRE1α cleaves GPC3 mRNA at a 3' UTR consensus site independently of ER stress, thereby prompting GPC3 mRNA degradation. Finally, we show that the expression of a miR-1291-resistant form of IRE1α abrogates the positive effects of miR-1291 on GPC3 mRNA expression. Collectively, our data demonstrate that miR-1291 is a biologically relevant regulator of GPC3 expression in hepatoma cells and acts through silencing of the ER stress sensor IRE1α
Reproductive characteristics and breastfeeding practices (N = 1291).
No full textReproductive characteristics and breastfeeding practices (N = 1291).</p
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